Scottish Doctor, author, speaker, sceptic

What causes heart disease part XXXVI (part thirty-six)

Wipe your mind clear of all previous ideas about CVD. About as easy as standing in the corner and not thinking about a tiger. In reality, once you have read about, and talked about, and researched, and thought about anything, patterns are created in your mind. Familiar landscapes develop, and well-worn pathways become the comfortable and easy routes to travel down.

Say what you like about Ancel Keys (and I had better not, for I would end up swearing a lot), he created the tightly patrolled mental box for everyone. Diet and cholesterol and cardiovascular disease. These are the great beacons that mark out, the map of the mind, where all thinking and discussion must take place. They illuminate all, and beyond them is darkness.

Now, blow out the beacons. Move out into darkness. We shall create a new landscape of thought. We have control of the vertical, and the horizontal, you are entering the Outer Limits. [I suspect some people may not get that reference]. We are breaking free of the box. In fact, there is no box, it no longer exists.

In the distance, there is a glimmer of light… it is our first fact. At least we hope it is a fact. We approach the glittering light and scrape way the grime that has been obscuring it for many years, to reveal…

Atherosclerotic plaques only develop in larger arteries.

Quite close to it, almost hidden away, lies another fact.

Atherosclerotic plaques never develop in veins.

There are two exceptions to the second fact – well, there are more, but these are the most obvious. First, if you take a vein, and use it to create a coronary artery bypass graft, it will develop atherosclerosis very rapidly. Secondly, if you create an arteriovenous fistula AV-fistula (fusing an artery and vein together) for dialysis patients, the venous section will develop atherosclerotic plaques.

Setting aside these exceptions, these two facts were as close to inarguable as I have been able to find. Inevitably, they lead to my first question. Why do plaques develop in arteries, and not in veins? Right now, I can see you doing what everyone does, searching for a simple answer, with thoughts such as:

There is less oxygen in veins, and oxygenation is damaging to arterial walls

The pressure is less in veins

The LDL level is lower in veins (it’s not, but I have heard a lot of people say this)

Arteries and veins have a different structure (they do not).

And so on, and so forth. Isn’t the search for a quick and simple answer fun…?

After exploring almost every avenue that I believed could possibly be involved in CVD, I found myself returning more and more often to the difference in blood pressure in veins and arteries as the place where the answers were most likely to be found.

However, I knew pressure, by itself, is not going to cause anything, unless you succeed in ‘bursting’ an artery, or ‘bursting’ the lining of the artery. I mean, this can be done. You can develop an aneurysm (thinned and ballooned area) in an artery, which can then rupture – usually with catastrophic consequences.

But before that, what can pressure do? Force things carried within the artery into the artery wall behind? No, that does not make sense. For that would mean everything carried in the bloodstream would simply be blasted into all artery walls, everywhere. The smallest molecules would go first, molecules such H20 to start with. Does this happen…. No, of course not. Our arteries, and the endothelial cells that line our arteries (and veins), are not leaky.

In short, differences in pressure cannot provide any sort of an explanation.

However, there is a law of fluid dynamics which says – words to the effect – if the pressure in a tube is higher, the velocity of the fluid flowing through a tube will also be higher. Which means that blood is travelling far faster in an artery than a vein. A veritable white-water maelstrom, compared to a meandering river as it approaches the sea.

Thus, it is easy to imagine that anything lining an artery is going to be exposed to far greater ‘forces’ than anything lining a vein. These forces, which I shall call biomechanical stresses, will be particularly intense in certain places. For example, where arteries branch (bifurcate) e.g. where the carotid arteries, that supply blood to the brain, branch off (bifurcate) from the aorta.

Another place of extreme biomechanical stress is within the coronary arteries. These arteries are exposed to a unique stress, in that they are compressed with great force when the heart contracts. Some have likened this to stomping on a hose every second. Indeed, blood cannot flow in coronary arteries during systole (ventricular contraction) because they are squeezed shut.

In general, if you look at where atherosclerotic plaques develop, you find that they most often occur at maximum biomechanical stress. Where carotid arteries (main arteries supplying blood to the brain) branch from the aorta, and also where other arteries branch from the aorta, and within the coronary arteries. It seems, therefore, that biomechanical stress is required for plaques to develop. This is not the same as high blood pressure, but it is closely associated with high blood pressure.

In truth, this idea is not in any way contentious. This is a highly jargon filled section from a paper called ‘Biomechanics of Atherosclerotic Coronary Plaque: Site, Stability and In Vivo Elasticity Modelling.’

‘Although the coronary and peripheral systems in their entirety are exposed to the same atherogenic cells and molecules in the plasma, atherosclerotic lesions form at specific regions of the arterial tree. Such lesions appear in the vicinity of branch points, the outer wall of bifurcations and the inner wall of curves. Pathologic studies, have shown that healed plaque ruptures are predominantly in the proximal portions of the left anterior descending (LAD), right coronary (RCA), left circumflex (LCx) and left main (LM) arteries. Investigations over the last decade have elucidated both fluid mechanical and most recently structural biomechanical factors that mediated the site of plaque formation.’1

Which is all fine and sensible. However, this very same paper states the following:

‘Plaque formation is now recognized as an inflammatory process triggered by high levels of serum LDL that enter the coronary wall, encounter oxygen reactive species, and become oxidized. The oxidization, in turn, stimulates the recruitment of monocytes that convert to macrophages to phagocytize oxidized LDLs. This forms a necrotic core with recruitment of smooth muscle cells from the media to seal over the fatty core.’

That is the official party line as to how CVD starts, and develops. But if you believe that, you immediately face a conundrum. How can you reconcile the hypothesis that raised LDL entering the artery wall initiates plaque development, with the observation that atherosclerotic lesions form at specific regions of the arterial tree? It is surely one, or the other, but it cannot be both. Sorry, but at this point I need to take you back into the landscape of raised LDL and CVD.

You may think, in fact you probably are already thinking: “Well, biomechanical stress damages the endothelial cells, allowing LDL to enter.” Now, that could be true. However, if that is true, then you have (if you believe in the cholesterol hypothesis), just made a move that will result in checkmate against you.

The argument goes like this:

If LDL can only leak into the artery wall at an area where the endothelial layer is damaged, and this is where plaques develop, this means it cannot leak through in areas where the endothelium is not damaged. Ergo, the first step in the development of plaques cannot be LDL ‘leaking’ into the artery wall past the endothelium, it is damage to the endothelium. Ergo, a raised LDL level is not the primary cause of CVD. Checkmate.

You don’t like that logic? If you prefer a few more facts, using a different approach.

If you think LDL is capable of, simply, transporting itself past the endothelium, then you need to define a mechanism. Is it simply osmotic pressure, with LDL travelling down a concentration gradient from the bloodstream into the artery wall? Is it actively transported through endothelial cells? Does it leak between the endothelial cells? These are the mechanisms that I have seen most commonly proposed – although they are often presented with so much surrounding jargon that it is almost impossible to work out what is being said.

In truth, I have spent years and years trying to establish if LDL can, or cannot, move into the arterial wall, past the healthy, undamaged, endothelium. If I had been organised enough, I could have gathered together ten thousand papers saying that it can, and another ten thousand saying that it cannot.

Having torn up twenty thousand papers, on the basis of complete uselessness, I began with, what may seem a simple question, a thought experiment if you like. Why would endothelial cells allow LDL to pass through them, to then allow LDL to be oxidised in the arterial wall behind? This process serves no physiological purpose, other than to kill you from cardiovascular disease!

The idea that endothelial cells simply cannot prevent this from happening is, frankly bonkers. Cells can quite easily control the passage of single atoms/ions through their cell membranes Indeed, this is one way that all cells function. To give one example, they can pump individual sodium ions out, and individual potassium ions in, to maintain an electrical action potential. They only lose the ability to control their own internal environment, within very tight parameters, when they die.

Therefore, the idea that an endothelial cell cannot prevent a relatively massive LDL molecule from entering the side facing the bloodstream, then passing straight though, then ejecting itself out the other side, is complete nonsense. Complete… nonsense.

Indeed, it has been well established that the only way LDL can enter a cell, is for that that cell to manufacture an LDL receptor, wave it about it the bloodstream to lock onto an LDL molecule, before dragging the receptor and the LDL back inside. Ergo, LDL does not get into an endothelial cell, unless the cell wants LDL to enter. It activates complex processes to allow this to happen.

The reason why some people have very high LDL levels is because they cannot manufacture enough LDL receptors, or the LDL receptors they manufacture are faulty. A lack of LDL receptors, or faulty receptors is, of course, the underlying problem in Familial Hypercholesterolaemia(FH). Proof, if proof were truly needed, that LDL cannot force its way into cells – no matter what the concentration in the bloodstream.

In short, even a superficial understanding of how cells control the passage of atoms and molecules, leads to the inescapable conclusion that LDL cannot possibly travel straight through an endothelial cell, without the activation of complex and highly controlled cellular process.

This problem has been duly noted by those who support the LDL/cholesterol hypothesis. So, the current thinking, although I have never seen it expressed clearly, is that there must be gaps between endothelial cells, wide enough for LDL to leak past.

Again, no. The fact is that, in a healthy artery wall, with healthy endothelium, there simply are no gaps between endothelial cells. Here, from a paper entitled. ‘Endothelial Cell Junctional Adhesion Molecules.’ [jargon alert].

‘Endothelial cells line the lumen of all blood vessels and play a critical role in maintaining the barrier function of the vasculature. Sealing of the vessel wall between adjacent endothelial cells is facilitated by interactions involving junctionally expressed transmembrane proteins, including tight junctional molecules, such as members of the junctional adhesion molecule family, components of adherence junctions, such as VE-Cadherin, and other molecules, such as platelet endothelial cell adhesion molecule.’2

At the risk of simply repeating what this paper says, there are no gaps between endothelial cells. Instead, there is a highly complex structure of proteins and other molecules between each endothelial cell ensuring that nothing gets past – unless the endothelial cells are instructed to let them past. This happens with white blood cells, they can open the junctions between endothelial cells, and move into the artery wall – then out again. Clever stuff.

Of course, if most things travelling in the bloodstream had to overcome complex barriers to get past the endothelium you would die, as your blood would simply circulate round and round, struggling to exchanging nutrients back and forth with the underlying tissue. Which kind of negates the point of having a circulatory system in the first place.

Nature, in the way that nature does, noted this potential problem, and came up with a solution. As blood vessels get smaller, and smaller, the endothelium develops holes – called fenestrations. These fenestrations allow almost everything present in the blood to flow freely in and out of the surrounding tissues/organs. Red blood cells would be one exception.

Why, you could ask, would endothelial cells have fenestrations in them to allow the free passage of molecules in and out, if things can freely pass in and out of non-fenestrated, tightly bound, endothelium?

At this point, I am overwhelmed with the need to make a quick summary:

1: It is impossible for LDL to pass straight through a living endothelial cell

2: Endothelial cells are tightly bound together, and will not allow anything to pass between them.

In addition, here are a couple of other facts to consider.

The first of which is that, in the brain, the endothelium never becomes fenestrated. There are no holes, even in capillaries (the smallest blood vessels in the body). Which means nothing can move into, or be removed from the brain, that the endothelial cells do not grant passage. This barrier function is usually referred to as the blood brain barrier (BBB):

‘Cholesterol is a major constituent of the human brain, and the brain is the most cholesterol-rich organ. Numerous lipoprotein receptors and apolipoproteins are expressed in the brain. Cholesterol is tightly regulated between the major brain cells and is essential for normal brain development. The metabolism of brain cholesterol differs markedly from that of other tissues. Brain cholesterol is primarily derived by de novo synthesis and the blood brain barrier prevents the uptake of lipoprotein cholesterol from the circulation.’ 3

To put this another way, if LDL could pass the BBB, then the brain would not need to synthesize its own cholesterol, and the brain does synthesize cholesterol within specialised glial cells. Which is further confirmation that an intact, non-fenestrated endothelium, blocks the passage of LDL.

Now here is a final fact (a final fact in this blog at least) that I would like you to ponder. Which is that large blood vessels have their own blood vessels, known as vasa vasorum. Literally, ‘blood vessels of the blood vessels’. Vasa vasorum surround and penetrate large arteries, and veins, supplying them with the required nutrients.

They are, of course, fully fenestrated (full of holes). Thus LDL, or anything else, can simply leak out of the vasa vasorum and into the artery wall if it so wishes – yes, even down a concentration gradient, if you like to think of it in this way.

Which means that there is absolutely no need for LDL, or anything else, to be absorbed through the endothelium lining the arteries, as it can get in from ‘behind’, so to speak. Which takes me back to my first question here. Why would endothelial cells transport LDL past themselves, and into the artery wall behind – if LDL can perfectly easily get into the artery wall from the vasa vasorum? This truly would be an exercise in pointlessness.

I could go on, as I have only touched upon a small part of the complexity involved here. But I hope to have given you enough food for thought. Yes, you easily can make statements such as ‘Plaque formation is now recognized as an inflammatory process triggered by high levels of serum LDL that enter the coronary wall’. Certainly, if you say it fast enough, and do not think about it, such a statement can seem reasonable.

However, if you start looking at the actual process required for LDL to travel into the arterial wall, you begin to realise that it is (with a healthy and intact endothelium) simply not possible. Or, if it is possible, it should be happening everywhere, in all arteries and veins. Not at discrete points.

At which point, you begin to realise that the cholesterol hypothesis, whilst is sounds superficially reasonable, requires mechanisms of action that just do not exist.

LDL cannot enter the arterial wall, at least not from the lumen of the artery, unless the endothelium has been damaged in some way. If you damage the endothelium, all hell breaks loose – and then we have a completely different story on our hands. One where LDL may have a role in plaque formation, or it may not, but it most certainly cannot be the primary role.

This is a conclusion that I arrived at a long time ago. Not, initially, because I set out to debunk the hypothesis. I simply wanted to understand how a raised LDL could cause atherosclerosis. ‘Because it does’, has never ever been a reply that I am happy to accept. In fact, nowadays I would translate this particular ‘because it does’ into ‘because it must.’ It must, because if LDL cannot pass through, or past, a healthy endothelium, the cholesterol hypothesis is wrong. And it can’t, so it is.

Now I have got that out of the system, I shall move on to look at what happens when you damage the endothelium. For that, logically, must be the first step in plaque formation.

Smarter sing
So diet and Stress are the causal factors, Like many I think that could be so, but I don’t see the mechanism. Human being S are adoptive, so why now, why haven’t we adapted to sugar and junk food. Also running around trying to trap your super must have been stressful

We only adapt in response to selective pressures that result in differential reproductive success. CVD typically affects older people who are past a typical reproductive age. We don’t adapt because a particular trait would be preferred, only where selective pressure exists.

Mr Chris, looking at ancient cave paintings, hunting seems to be celebrated and enjoyed, perhaps as many today enjoy team sports.

I doubt that the life of a hunter-gatherer was idyllic but it was far better than the servitude that came with staying in one place and growing crops. The evidence suggests a sharp decline in our ancestors’ health following the move into crop growing. Europeans who met hunter-gatherers often commented with envy about their perceived easy life and good health.

Thank you ! The facts are very clear and well expressed. I have come to the conclusion that medical people who believe that LDL-C causes CVD, are simply people of a non scientific medical faith. The profession has been captured by such faiths before. In the 19th century there was all the brouha about the significance of bumps on the human skull. What was that nonsense called ? I cannot remember. Never mind. Now that is seen as a sort of ‘joke ‘.

For light reading I am delving into a biography of Arthur Conon Doyle : “Teller of Tales ” by Daniel Stashower.
Conon Doyle was a medical doctor with in his early years a practice in Portsmouth. Conon Doyle is quoted as stating ” Science is the consensus of opinion of scientific men ( sic) and history has shown that it is slow to accept a truth. Science sneered at Newton for 20 years. Science proved mathematically that an iron ship could not swim and science declared that a steamship could not cross the Atlantic.:”

Lots David! He spent the last 20-30 years of his life believing or at least thinking they should be investigated..And he was not alone at the time. Many famous people shared his views.
I skipped a good deal of those chapters. But he was still a good author & writer in many fields over a long period. And he took up a number of good & worthy causes to achieve reform. He died at 71 of a heart attack in 1930. I suspect that he would have survived longer if he had used his considerable research skills to investigate the causes of heart disease.

I might be completely wrong here but my engineering logic tells me that the narrower a tube is the higher pressure is needed to get the blood flow through. Thus it must in my mind be the capillaries that requires the high artery pressure. On the venous side there is lower pressure requirement by the same logic.

Yes, the pressure drops with higher velocity (Bernoulli)… but that is relative to the starting pressure.

More apropos I think is that the circulatory system is essentially a closed system (in a short time frame anyway). The total volume of blood flowing into arteries has to be the same as the total volume being returned by veins. There is a pressure differential due to work having to be done to circulate the blood (particularly the work of getting through the capillaries), so arterial pressure must be higher than venous pressure or the blood wouldn’t circulate.

But as far as velocity goes, is depends on the cross-sectional area of the arteries vs. veins. If the total area of the arteries is similar to the total area of the veins, then the arteries will be higher pressure, but similar flow rate, as the veins.

(I have no idea what the relative areas are, and it isn’t a simple question the further you move from the heart, as pipes bifurcate and get smaller.)

If the arteries of the heart itself are of similar cross sectional area to the veins, then the significant difference between arteries and veins is pressure, not flow rate. Again, I don’t know how the areas compare. (Actually, the heart is two different pumps, pulmonary and systemic, which would need to be considered separately.)

Cross sectional area of arteries is considerably less. I suppose this can be argued the other way round, in the the heart has to pump at high pressure to create sufficient force to get the blood through the body. So, the arteries have to be narrower than the veins, with thicker artery walls, to deal with this pressure. [A lot of the ‘pumping effect’ is created by arteries expanding, then contracting, forcing the blood down them]. Does this work as a concept?

In the arteries it can be modelled to a first approximation as a pump forcing a liquid through a system of tubes, losing pressure to friction on the way. The expansion and contraction of the arteries could be due to simple elastic stretching under pressure and relaxing as the pressure pulse passes, or if it is assisting the blood flow, it must be putting energy into the system for which the artery muscles must be burning fuel. It would be interesting to know what percentage of resting metabolism goes into arterial pumping, if any.

Veins work differently. They are flexible tubes with one-way flap valves, so if they get squeezed anywhere along their length by muscle action, blood flows towards the heart. In theory they don’t need a pump or pressure differential to operate. Whether the muscle action is contributed by the venous muscles contracting and relaxing, or by body muscles pressing against the veins and squashing them, or a combination, I don’t know.

Flow in the capillaries I’m guessing is rather more complicated. Here the fact that blood is not a dead fluid like water moving through inert pipes, but a living assemblage of molecules and cells moving through a biologically active tube means that micro-mechanical and electrical forces play a far more dominant role that simple hydraulic pressure and friction. I leave it to others to explain.

From observation, if you scratch yourself the blood just oozes out, telling me there is almost no pressure differential in capillaries in body tissue. You have to cut pretty deep to get any significant flow of blood.

Martin Back: When I get a minor wound the blood doesn’t ooze out; it flows freely. I recently had mohs surgery, and I bled so freely the surgeon asked me if I was taking blood thinners. Should blood ooze out?

Since (see Dr. Kendrick comment) the cross sectional area of the arteries is significantly less than the veins, then fluid velocities in them will be higher. Therefore it certainly could be that turbulence is more likely to occur, usually at places like bifurcations and the inner radius of loops.

But fluid flow and turbulence is a difficult thing to generalize – careers have been spent studying it. Part and parcel of studying/modeling fluid flow is the shear stress problem. Add to that the biological effects, particularly as Martin points out in the capillaries, and this is a tough nut to crack.

But back to Dr. Kendrick’s original thought, “… that blood is travelling far faster in an artery than a vein. A veritable white-water maelstrom, compared to a meandering river as it approaches the sea.”, I would simply comment that it certainly is plausible that the higher fluid velocities, coupled with mechanical disturbances such as bifurcations, could lead to the conditions (mechanical/fluid/biological) which would cause endothelial damage and the cascade of follow-on affects.

Perhaps a some promising young fluid-dynamics researcher could make a career teasing out the specifics of this topic….

John you wrote, “Perhaps a some promising young fluid-dynamics researcher could make a career teasing out the specifics of this topic”

Bugger that mate. Too long winded; far too trusting ! And pius as well. Having buggered us all around with their cholesterol hypothesis for decades, you dare suggest that we just wait again ? So the researchers & company backers can have just another chance at fame & fortune ?

Really ? I think that is BBB ( Bullshit Baffling Brains )

Most of us here are interested in this issue so as to ease a urgent disease we or our families face in right now.

Together I believe we together will crack it. Our collective thinking, researching the web, personal experience, purpose, energy and commitment, lead by Dr K. can do it far quicker and cheaper and be a benefit of far more ordinary people.

Hmmm………..do I detect a modicum of excess stress? Apparently not good on an individual basis, but; worrying about disease at local level distracts from the “disease” which afflicting the world, which is over population. The growth cannot continue indefinitely, and the longer the growth continues the greater will be catastrophy when it arrives. There is enough information in these blogs for people to make a change (if necessary) to a less risky lifestyle, but that should be for quality benefit not just expecting to live longer which in turn contributes to the over population.

AH Notepad: On the other hand, sperm counts are down 50% over the last 50 years, and fertility is below replacement level in Japan and some European countries. The population problem may very well take care of itself.

Sasha: I haven’t, and haven’t given it a lot of thought, but toxic chemical load probably plays a large role. Increasing nutrient deficiencies in otherwise well-fed people. The measles vaccine came into use fifty years ago. Modern medicine has played a much smaller role in their lives. Nuclear fallout and fluoridation have largely been confined to the north temperate zone. Probably less social displacement. Any ideas?

In physics there is this principal of ‘conservation of mass’. It means that if two pipes have the same diameter (arteries and veins perhaps?) and carry the same fluid, the flow in both have to be the same. This would mean that the flow in the arteries can not be higher than in the veins, unless one is smaller (has a smaller diameter).
Another principle is that the flow through a pipe is a (mostly not linear) function of the longitudinal pressure gradient. This explains why the pressure at (the begin of) the arteries can be much higher (you say 20 x) than in (the end of) the veins.
If you take the end of the veins as a reference, going ‘upstream’ means going against a pressure gradient. So pressure naturally builds up from the veins to the arteries.
The assumption being that the heart is providing this pressure (or sucks at the vein’s ends, but that would probably collapse the ‘hose’).

Blood pressure is, normal, about 120/70 in major arteries (BP goes up and down as the heart contracts and relaxes. Maximum pressure 120mmHG (millimetres of mercury), lowest pressure it falls to 70mmHG) When it reaches the capillaries, smallest blood vessels, pressure is considered to be 0mmHg. Pressure rises a bit as the blood travels back to the heart capillaries > venules > veins. Max pressure about 8mmHg.

Pressure in the lungs is much lower. About 20/8mmHg in the arteries. About 15/2mmHg.

I for one know that the blood flow to the heart muscle itself can be problematic especially if I would try to run which I very seldom do for good reasons.

Still I remember getting into Dr. Srokas teaching and had a link to a cardiograph video showing a totally blocked LAD like my own and where there was an evident backfill of the artery “downstream”, i.e. on the down side of the blockage, an irrefutable (?) proof that natural by-passing had occurred.

Thus, the micro-vessels evidently do their job which supports my continuous CABG refusal. Still my blood pressure is 110/60 at rest. Does this make sense?

to Bill in Oz: Wow. You seem to be throwing all research into the same basket: misleading, conflicted interests, misused, … etc.

And then you suggest “researching the web”. That made me smile – if you find a useful nugget of understanding about what causes CVD on the web, where do you think it came from? Other than the few things we can sense directly, it came from research somewhere, sometime. I know I can’t feel my own arterial endothelium or its condition, so no matter how committed, experienced, or energetic I am, I would never be able to figure out the root cause(s) of CVD from what I personally experience (nor could anyone else). But research can tackle such questions, albeit in the real world with may stops, starts, wrong paths, etc.

I agree that much (perhaps even most) “research” get misused by companies with financial interests. But that doesn’t change the fact that good quality fundamental research has added, and continues to add, to the sum of human knowledge. An understanding of the dynamics of fluid flow in the circulatory system is such an area that I presume would benefit from some good basic research.

For answers to the CVD epidemic this week, or year, or decade, studying lifestyle habits around the world is very likely a much more practical approach, but we can say that because research (oh oh, there’s the “R” word again) into different populations around the world has shown us that CVD is an anomaly, not the norm, of the human condition.

Even if we could come up with a lifestyle prescription to greatly reduce the prevalence of CVD in modern society (did someone say Primal?), you are *still* no closer to understanding the actual bio-chemical mechanism for CVD. You’ve just found a formula to avoid it. Which is great – let’s do it. But understanding the underlying biochemistry as well could have benefits even far exceeding reducing the incidence of CVD. And that takes research.

John, you wrote ” You seem to be throwing all research into the same basket: misleading, conflicted interests, misused ‘

No John, that is absolutely NOT what I am doing. I am using the web, It is a resource & a mass of information. But I suggest we all need to be careful with it’s use.

The article that Goutboy suggested we look at, I looked at with an open mind. But the first step in analysing it is to examine the assumptions behind it,
In the discussion toward the end, the authors state that the following 7 sources “demonstrate” that LDL-C penetrates the artterial wall and causes CVD.

I examined each of those 7 sources. And none of them ‘demonstrated’ ( ie proved ) their assertion. In fact some of them were irrelevant; some proved the opposite.

The article was a house of cards. It collapsed. And the authors were attempting ‘scientific fraud’. I am still surprised by this as I did not expect it to be so blatant; so shoddy.

But now we have this new 20 year scientific study from Western Scotland on the use of prevastin. Let’s see what real science is here and what insight it offers.

WOSCOPS produced a 2.4% reduction in MI and death from MI. I suspect a switch to a Med diet or better still a whole food plant based diet with some wild fish would produce far better results, it certainly did in the the Lyon heart study (think I got that study ID right, correct me if not). Now how many GP’s tell a patient you can eat lots of delicious WFPB food and fish and slash your risk or you can take a pill and merely reduce your risk ?.

Smartersig, I agree absolutely, the Mediterranean diet is far far better….But as I state in my other comments on this Prof. Ray’s research paper, the placebo group after 20 years, is no longer a ‘placebo’.

The phenomenon of Blood Pressure Amplification occurs where the arterial pressure increases as it travels to the periphery, but flow decreases. That’s why we should be measuring central aortic blood pressure and not the BP in your brachial artery as this just gives you an indication of the pressure in your arm. This also accounts for the design and physiology of arteries that change from more elastic large vessels like the aorta to more muscular anatomy in the peripheral arteries, that act as an additional pumping mechanism to that of the heart. When the central and peripheral arteries “harden” and lose their elasticity, BP rises which is necessary to maintain flow.

Have to be watch simplifying your models too much. Medicine thinks of circulation as as simple pump and tubing. High pressure generated in the left ventricle, low pressure in the right atrium, therefore blood flows between the two. However, the pressure in blood leaving the capillary system cannot possibly be higher than that in the right atrium, particularly if you happen to be standing up, so there is no clear reason for blood to flow from capillaries back to the RA. Thus I suspect something else is involved, something quite significant.

On the issue of pressure/turbulence/bio-mechanical stresses being involved in the location of arterial plaques . . .
Recently I read a paper “Hypothesis: arterial glycocalyx dysfunction is the first step in the atherothrombotic process” https://www.ncbi.nlm.nih.gov/pubmed/18319293 FREE

Some of its points:
“Blood flow in arteries is associated with a shear stress at the glycocalyx, which signals the underlying endothelial cells to release nitric oxide (NO), an anti-atherogenic factor.”

“Sites of low shear stress in the arterial tree are more susceptible to atheroma due to lack of NO generation through this mechanism, whereas exercise, by increasing blood flow and shear stress, is protective.”

Counter intuitively the sites of least surface shear stress are the bifurcations in arteries where there is turbulence. (I would also guess that the inside curve, rather than the outer part, of an arterial loop would have lower shear shear stress and guess plaques should form there.????)

They seem to be saying that protienaceous hairs extend from inside the cytoplasm of the endothelial cells into the protective glycocalyx, and it is these that stimulate the production of protective NO, relaxing the smooth muscles – but mainly where the shear stress is high – where the NO need is highest??

I ponder on . . . why are veins, one assumes with super low shear stress . . . are not jammed with plaques? Perhaps they do not have the same demand on them as arteries, so are less needy of NO?

Bill, on shear stress . . . In my rough take on shear stress: . . . If you rub the palm of one hand over the palm of of the other hand you can feel the effect of shear stress. If you do it quickly the shear stress effect appears greater. The faster the flow the greater the sheer stress.

If you stand by a weir in a small fast flowing stream and you are able to put your hand in the middle you can feel the feel force of the stream rubbing against the hand. In contrast, at one downstream corner of the weir, where the flow was disrupted (turbulent) it would not be surprising to find calmer areas where forces are less. I can see that turbulence does not necessarily mean high shear stress.

Ahhhhh ! Thank you Anthony. When a good deal younger I used to swim in a river with rapids for the thrill of it. Usually my mates & I would carefully make our way to the head of them and then dive into the current and swim in the fast current to where it petered out and curled back in a loop which would take us back upstream again. But for the fun we would occasionally swim furiously against the main current. Then I felt the shear stress of the water.

Wall shear stress is the effect of friction from the flowing fluid on the wall. The cells must resist this or be displaced. It is not the only stress. Fluid pressure exerts a tensile stress to limit the artery expansion and asymmetric loading from flow not contacting the wall the same on both sides apply a shear force in the wall also. These branches are not perfectly uniform in cross section or branch angles. The artery is attached to underlying muscle as well. The artery will want to twist. This is what applies the additional shear force. It makes these high stress areas. Obviously the design is sufficient in most instances. If you change the elasticity, increase the stiffness, overtime this may lead to damage. The repairs, plaques, then cause the stiffness to increase more. There is a monkey study on this I read last night. Diabetes decreases elasticity of the artery. Stress hormones expand them. My two cents anyway.

Steve, this article has a very curious conclusion :
“This data suggests that arterial stiffness in combination with minimally invasive parameters can be used to predict the severity of diffuse asymptomatic atherosclerosis in MONKEYS. However, more widespread application of this data to humans is uncertain because of biological variability and differences between animal models and human subjects.”
God bless the monkeys. 🙂
No such blessing for us humans. 😦
Now what was I thinking of…..

What I meant to say in my reply a bit above, is that the statement by Dr. Kendrick,
“However, there is a law of fluid dynamics which says – words to the effect – if the pressure in a tube is higher, the velocity of the fluid flowing through a tube will also be higher. Which means that blood is travelling far faster in an artery than a vein.”
is not correct. It’s not the pressure in the tube which determines the speed of the flow, but the pressure difference across the tube.
And that the blood in the artery can not travel far faster than in the vein, unless the diameter of the artery is far smaller than that of the vein.
Physics 101.

Yes, you are correct, about fluid dynamics, in a pumping station probably. Perhaps I should have been more precise. Arteries are, generally, of lesser diameter than veins. Also, pressure drop from heart to capillary is far greater, than pressure in veins, so flow will be more rapid. We know that pressure is far higher in arteries, and that blood blow is also far faster. One must also be careful, because arteries and veins are not simply tubes. They react and expand, and contract and suchlike.

quote:
“When it reaches the capillaries, smallest blood vessels, pressure is considered to be 0mmHg. Pressure rises a bit as the blood travels back to the heart capillaries > venules > veins.”

It seems physically questionable to me that pressure would be zero at the capillaries, because how is it then supposed to return to the heart? It would imply that the heart has a negative blood pressure then, sucking the blood through the veins away from the capillaries.
After all, a pressure gradient is imperative in order for the blood to flow.
Also, the statement that “Pressure rises a bit as the blood travels back to the heart…” seems equally strange as that would imply that the blood would flow from the heart rather than to the heart.

Harry. Ask yourself this question. How does the blood flow back to the heart, if the pressure in capillaries is, effectively zero? The heart most definitely pumps blood into the tissues and organs, but what brings it back again? It is a fascinating area, and clearly does not operate according to a simple pressure gradient, out of the heart and back in again – down a gradient.

The heart by itself doesn’t have enough strength to pump blood through the rest of cardiovascular system, does it? I thought that there’s contraction in the blood vessels themselves to help move it along.

@DrMalcolm: I now understand that the reality of blood flow is much more complicated than the seemingly simple model you presented at the start of your article. From Andrew Larwood’s contribution I learned that even the arteries themselves are pumping through muscular action. Also, arteries are flexible ‘pipes’.
Sorry, but with my quite rigid background in physics I simply couldn’t accept the statement that ‘if the pressure in a tube is higher, the velocity of the fluid flowing through a tube will also be higher’ because it’s simply not true.
But if you add flexibility and muscularity of the arteries and veins, capillary actions and the non-Newtonian properties of blood together with the pumping actions of the heart then apparently all kinds of surprises are possible.
Let me add that I do love your articles, especially your colloquial writing style and strict adherence to logic. Thanks.

Thank you. Summer holidays being over, I am back to getting the old brain cells up to speed, and part XXXVl certainly does the trick. All so logical.
As Smartersig states today, I believe that what we eat is a main player, and ultimately, we mortals can have some say in that. However, the in-depth explanation of anatomy and physiology, as described by Dr Kendrick, is a great help to me. I must admit, reading such good work, further discourages me from attending my GP’s surgery, as it widens the gap of the status quo as practiced in today’s NHS regarding this type of logical thinking. Such a discussion with the Practice Nurse would, I fear, be time constrained at best, and pretty futile at worst. And don’t mention talking to the GP….I don’t want my other ear bitten off, as happened to the first one a few years back.
So, back to the healthy food practices I am following.

I do note that although the cells in the artery walls are tightly bound you also describe a mechanism where the binding can be loosened to allow white blood cells through.
So there is a way of sorts.
A bit like a bouncer on the door of a nightclub?
No problem, we are very selective. 🙂

You also describe a way that artery walls can develop fenestrations to allow nutrients out into the tissues where this is desirable.
Although not in the major arteries.

So to me this does open two possible avenues (included in arterial wall design) where a defective mechanism in the walls of the major arteries might allow small particles to work their way through the walls.

I also note that you cover this off by suggesting that if the walls start leaking then you have a world of hurt. Presumably because a lot of stuff would leak before the LDL particles got a look in. Although I am not sure if this explains the movement of white blood cells.

Thinking, the IMA ( mammary artery) is grafted upside down on LAD blockages and rarely get damaged…. think think think! “Only rarely was an atherosclerotic change observed in the IMA. In our study, 2 of the 18 grafts examined 5.22±4.76 years following grafting, it was described as “small focal, infiltrates of lipid in the intima”.”…”Endothelial cells of the IMA are rich in heparin sulfate and endothelial nitric oxide synthase (eNOS), and release a greater amount of nitric oxide (NO) that contributes to the antithrombotic properties and endothelial homeostasis which confers protection from atherosclerosis.” ( am i getting close??) Post menopausal women do worse with CABg, maybe eNOS problem. Is it to do with elasticity of IMA + NO + Anti thrombotic factors… why does the Saphenous Vein become problematic, sometimes full of plaque at a year??? Thinking still….reading: http://www.annalscts.com/article/view/2416/3282

@SW, Reading the article, and the table comparing the properties of the IMA and SVG, in the latter the larger number of fenestrations, higher intercellular junction permeability, high dependence of vasa vasorum (which I guess are no longer around once grafted and presumably have a part not only in supplying things to the vessel but also removing?) and lots of other factors would seem intrinsically problematic – aside from the fact that it was originally a vein and is then expected to become an artery. Incidentally, you say it’s grafted ‘upside down’ – is this relevant at all, I wonder? I’m not really surprised that the SVG doesn’t really do the job very well.

Thank you, Malcolm. Clear and logical as always. I smile every time one of your blogs pops into my inbox because I know how much I am going to enjoy it. I am sad at how many people still say ‘I am treating myself to X, Y or Z today, but I don’t usually of course because of cholesterol’. These false ideas cause so much anxiety. Thank you for working tirelessly to challenge them.

Not entirely sure why, but I was reminded of Neil Gaiman’s American Gods. How people cling tightly to beliefs because they feel they will cease to exist if they don’t. Analogy may not be quite right but its there somewhere!

I can see why you need to ask what happens when the endothelium gets damaged, but isn’t the million dollar question – why?

This might provide only meager food for thought, but when I’m working with clients, I always try to frame disorders as a system overly taxed. Anxiety is super useful in keeping us alert and doing what we need to do in order to survive, but when adrenaline is surging too often in too great a quantity, the system adjusts upward and finds homeostasis at a unhelpful level. It might have been useful in the moment (evolutionarily to outrun the sabertooth tiger), but over time, it is entirely deleterious. Same goes for depression, which is likely a signal our brain is receiving from the environment that it’s time to retreat and be safe. But then the signal is too strong and the retreat is too complete. I assume that the system of repair is similarly useful for our arteries, but then it becomes overtaxed and all hell breaks loose. Perhaps there is even some homeostatic state that is achieved that is also unhelpful (until it is reversed with proper diet, exercise and stress relief).

What an enjoyable read – devastatingly convincing logic, clearing away a lot of the brushwood and undergrowth surrounding the pathogenesis of atherosclerosis. . . ready to move on.

This is just one of many highlights . . .

“The reason why some people have very high LDL levels is because they cannot manufacture enough LDL receptors, or the LDL receptors they manufacture are faulty. A lack of LDL receptors, or faulty receptors is, of course, the underlying problem in Familial Hypercholesterolaemia (FH). Proof, if proof were truly needed, that LDL cannot force its way into cells – no matter what the concentration in the bloodstream.”

I read and admired the work by Nobel prize winners Brown and Goldstein nailing the LDL receptor, but I was not comfortable with the work being used as a proof of cholesterol as the prime mover of CVD. For one, you were dealing with a very specific genetic defect in a limited number of people so I always wondered how generalisable their biochemistry would be to the rest of the population.

And for two: when they wrote about their paper saying it showed high cholesterol was the cause of CVD . . . I shouted out (literally) “No! it showed there was an association”

So, Malcolm, there was a sort of poetic justice that the FH work provided an excellent coup de logic against the idea of LDL as the prime culprit.

Very good. But what causes endothelial damage to begin with? I’m beginning to believe that CVD (and cancer for that matter) are not caused by just one thing, but various things – much like all of the car accidents in the world are not caused by one single thing.

The scientific human mind wants singular causality for almost everything. Are you obese? Must be sugar (or Heaven forbid, fat). Climate change? Must be man. Heart disease? Must be high cholesterol. It’s simply easier for our simple minds for 1+1 to equal an easy answer.

I think you’re right. Nothing has a simple answer. I think that sugar/high carb is a major (if not THE major) factor in obesity, but I also think Omega 6 fatty acids (of the plant oil variety) are also a large factor. (Any prepared food in the US usually has both of these.) I even think “exercise” is a factor, even though I personally have lost a lot of weight while decreasing exercise. However, many years previous to this, I also ate a very low fat diet that was OK as long as I exercised a TON. As soon as I got injured, I gained weight immediately. I also lost some pounds when biking 60-100 miles a week during the summer, although I think this was due to biking causing reduced blood sugar and a change in insulin resistance, not due to calories. (And, once I stopped biking like this, I gained all the weight back very quickly.) Factor in genetics (why can some people not gain weight even eating high amounts of carbs, but if I look at carbs I gain weight?), etc., and you end up with an overwhelming number of factors.

However, when I tell my kids what to eat to control their weight, it’s the following (with 1-3 the most important):
1) Avoid sugar;
2) Avoid seed/vegetable oils;
3) Avoid all grains;
4) You may have to eat less or no milk products, or eat sparingly;
5) You may have to avoid high Omega 6 foods, such as chicken and nuts, or eat sparingly;
6) Exercise is probably immaterial (for weight loss);
7) Vegetables and some low carb fruits might be OK, but they may not be beneficial or could possibly be detrimental;
8) Fiber is probably detrimental;
9) Resistant starch/probiotics may or may not be beneficial (though my 3-4 month test of these indicated they were not beneficial and may be detrimental).

I think this pretty much covers everything I’ve learned in 4+ years of my own nutritional journey, and is, of course, subject to change at any moment (eg, due to new data/information or tests performed on myself). 😉

I watched an episode of a TV documentary Inside Natures Giants, about the whale. One researcher commented on the clean blood vessels around the heart. Whales eat protein, fat and sea vegetables. Their blood glucose and insulin levels would be stable, in the healthy range.

IT is akin to the human factors we use in aviation, the Swiss Cheese model. When airline accidents happen all the ‘holes line up’. It is never just one thing, totally agree. I don’t think there will be a ‘unified theory’ of CVD….

Great article? I have a couple of general questions? Does atherosclerosis equal calcifications, i.e. such as seen on CAC imaging? I’ve heard that the CAC only shows the “hardened” plaques but this is preceded by “softer” plaquing that is not yet readily seen on CAC scanning? And, what about what is incidentally seen in the femoral or iliac arteries when pelvic CT scanning is done? Isn’t atherosclerotic plaque the cause of peripheral artery disease? How does the proposed mechanism of “squeezed” arteries explain peripheral arterial plaque formation?

“At which point, you begin to realise that the cholesterol hypothesis, whilst is sounds superficially reasonable, requires mechanisms of action that just do not exist”.

I have been collecting examples of ways in which such assumptions are made: mechanisms that are necessary for certain theories, but which turn out (on the most superficial inspection) to be impossible.

Take, for instance, the underlying axioms of classical economics: (1) that individuals are perfectly rational; (2) that they maximize their utility, benefit or profits; (3) and that they act independently of each other, on the basis of perfect information. All of those are provably, indeed obviously, quite untrue. But those axioms must be adopted if classical economic theory, and its tidy little equations and models, are to work! Hence they must be accepted.

To my mind, the aphorism that ties all this together is Robert A Heinlein’s warning: “Man is not a rational animal. He is a rationalizing animal”. In other words, we do not usually start by seeking the objective truth for the good we may get out of it. Instead, we start by asserting things that we would like to be true, and make up rationalizations for them.

Sorry about this. I’m posting just so I can try getting comments again. I am getting Dr K’s new posts, but not being notified of any new comments. I had this problem with the last post. I’ve tried clicking ‘follow’ but it says (obviously) I am already following. Has something changed perhaps? Can someone tell me if they are notified every time e someone posts a new comment – or is it just me?

The main cause of endothelial damage was discovered during the 1980’s by the late, two times Nobel prize winner, Dr Linus Pauling and Dr Matthias Rath. They published their findings in a paper “A Unified Theory of Human Cardiovascular Disease Leading the Way to the Abolition of This Disease as a Cause for Human Mortality” in the Journal of Orthomolecular Medicine Vol. 7, No. 1, in 1992. But was ignored by mainstream medicine for decades.

There is of course a blog on vitamin C, but the index on the right is a bit too short. You can find it here https://drmalcolmkendrick.org/2017/01/28/vitamin-c-an-update/, where you will find the usual standard of revelations hidden and/or ignored by mainstream medicine, pharmaceutical companies and their media run by such notables as R. Slickers.

“Turbulence or turbulent flow is a flow regime in fluid dynamics characterized by chaotic changes in pressure and flow velocity. It is in contrast to a laminar flow regime, which occurs when a fluid flows in parallel layers, with no disruption between those layers” (From Batchelor’s Introduction To Fluid Mechanics.)
Surely, Mr Bernoulli has his effect on the inner surface of arterial curves. I can easily visualize a chaotic change “pulling” an endothelial cell apart because of momentary very low pressure – even on such a tiny scale – caused by turbulence.

Brilliantly written but none of it takes into consideration the history of the disease. Death by heart disease is fairly modern and fairly western. Something happened in the early 1900’s that dramatically increased the rate of heart disease and resulting death, but what?

Sure, plaque can be found in “some” mummies dating back thousands of years but there doesn’t seem to be anything from the literature of the time that implies any deaths as a result. There is also nothing to imply that commoners had plaque.

No doubt there has been a heart attack or two throughout history but modern epidemic exploded in the early 1900’s. What caused it and why? The cause can most likely be found in those two questions. High blood pressure, cholesterol and all the other suspects existed long before the explosion at the turn of the century.

Hebreden accurately described angina and death from MIs, three hundred years ago. This, of course, does not tell us how common it was, but it does not seem to have been uncommon. My own view is that it is very difficult to know what the rate of CVD may have been in the past, but that it definitely existed. Virchow and Rokitansky were arguing about the cause of atherosclerotic plaques in arteries in the 1850s.

Was there an explosion of CVD in the early 1900s? Personally, I do not believe that this statement can be made.

The death rate was 202.2 per 100,000 in 1900. It climbed to 355.5 by 1950 and started a decline to 192.9 by 2010. I call that an explosion. On top of that in the US the rates can run from a little over 100 to a little over 1,000 per 100,000 today depending on where you live. In the early to late 1800s most Americans lived on farms or farmettes with access to “real” food and very few chemicals. From 1900 to the 1950s most Americans had left the farms. By 1900 wheat millers were degerming wheat removed the vitamin E and B6. Correlation my not be causation but part of the puzzle may be solved by looking at the timeline and major changes on that timeline…

My grandfather’s death certificate showed acute indigestion (go figure). Though I misquoted the numbers for 1900, all chart I have been able to find show death from heart disease as the 4th to 6th leading cause. I have not seen where heart disease was not a diagnoses until 1948.

CHD was not a diagnosis in the US until 1948 when they agreed to use the International Classification for Diseases system. That is just a fact. Heart disease was a ‘catch all’ term, used up until that point.

The following is a quote from Hebreden’s writings. It really does not sound like angina to me, “Yet it is not to be denied that I have met with one or two patients, who have told me they now and then spit up matter and blood, and that it seemed to them to come from the seat of the disease. In another, who fell down dead without any notice, there immediately arose such as offensive smell, as made all who were present judged that some foul abscess had just then broken.”

Dr Weston A Price and others documented that “primitive” peoples eating their traditional diets didn’t have “diseases of civilization”, but when they began to eat the “Western” foods such as flour and sugar, those diseases showed up within a few years. To my mind that is fairly convincing.
It’s an interesting historical pattern that, from the beginning of agriculture, farmers and the ordinary people began eating grains and domesticated foods, and lost the wide variety of wild foods (and especially meat) that hunter-gatherers enjoyed. There is a lot of evidence that their height and health declined immediately, and they bagen to suffer far more diseases.
With one exception: royalty, nobility and the gentry. Traditionally their recreations have been huntin’, fishin’, and more recently shootin’. Consequently they could feast on wild venison and other game, together with cheeses and fruits, while the lower classes had to make do with bread, root vegetables, and smaller amounts of domesticated meat. (In the Middle Ages, it was usually a capital crime to poach “the King’s venison”).
Nevertheless some kings managed to dig their graves with their teeth. In England alone, one might point to William the Conqueror (whose coffin was so heavy it couldn’t be lifted), Edward IV, and Henry VIII. I suspect that sweets and pastries must have played a part, as well as alcohol.
Then again, modern life is full of other hazards as well as bad diet. Air pollution, the masses of dangerous chemicals in air, water, food, drink and everything else, stress, etc.

You are so correct Tom.
Have you cast an eye on the rubbish being put into the wheelie bins used to collect food for the food banks in England? I kid you not…..the food collection bins at our local libraries are, indeed, the same as used for our garbage every week, ( clean, of course). The poor don’t stand a cat in hell’s chance of getting nourishing food into their bellies, just as in centuries gone by. If it wasn’t for the fact that kind-hearted people put the processed food into the collection bin, and the hungry need to eat anything passed on to them, I might suggest they cut out the middle man( the poor, hungry recipients) and take the bin direct to the tip. Or is that too political?
Processed food is far from what the needy require, but nice folks feel they are doing their bit by depositing cornflakes etc in the receptacles. Fresh, wholesome food cannot be stored and thus distributed safely……so give the needy the money to collect good stuff from the supermarket…..SIMPLES!!!

Jennifer: Here in the U.S. the postman puts out and picks up bags of this junk, as do the disease charities. I never contribute, not out of spite, but because it is complete junk. Lots of hungry people here, but this is killing them faster.

Apparently 42 MILLION hungry souls in USA, according to Feeding America. Most affluent place on planet earth. Huh! And here in UK, we are no better. I repeat my moan….even those getting fed are malnourished.
I wonder how much exposure the Archbishop of Canterbury gets today, regarding The Commisson on Economic Justice. ….I had to get a half decent report in the Irish press yesterday, but eventually it is filtering through to BBC.
What a damn disgrace.

I have been rereading Gary Taubes’ invaluable “The Diet Dilemma” (a stupid title imposed by his UK publisher instead of the far better original US title “Good Calories, Bad Calories”). On pp92-3 of my paperback edition I saw these passages:

“In a 460-page report entitled Physiological and Medical Observations Among the Indians of Southwestern United States and Northern Mexico, [Ales] Hrdlicka described his observations from six expeditions he had undertaken. ‘Malignant diseases,’ he said, ‘if they exist at all – that they do would be difficult to doubt – must be extremely rare’. He had not encountered ‘unequivocal signs of a malignant growth on an Indian bone’. Hrdlicka also noted that he saw only three cases of ‘organic heart trouble’ among more than two thousand Native Americans he examined and ‘not one pronounced instance of advanced arterial sclerosis’. Varicose veins were rare, and hemorrhoids infrequent. ‘No case of appendicitis, peritonitis, ulcer of the stomach, or of any grave disease of the liver was observed,’ he wrote.

“Hrdlicka considered the possibility… that these Native Americans were unaffected by chronic disease because their life expectancy was relatively short; he rejected it because the evidence suggested that they lived as long or longer than the local whites”.

Tom, the Royal Naval surgeon, T.L. Cleave, who features in Nina Teicholz’s excellent book, believed that sugar, flour and refined carbohydrates destroyed the health of populations introduced to such foods, as we were at an earlier stage.

Published in 1974, his book contains a great deal of sense that was nearly sunk without trace by the idiocy of the low-fat diet.

If people dropped dead from heart attacks in the late 1500s, you would expect Shakespeare to make use of the fact. But it seems not.

In a charming article titled, “Shakespeare as Health Teacher,” from a 1916 issue of The Scientific Monthly, James Frederick Rogers, M.D., writes of the Bard: “A curer of disease he certainly was not, but as teacher of mental and bodily sanity he has had a clientele that is numberless.”

10 deaths from strong emotion are recorded by Shakespeare (three occur on stage); all are due to grief, typically at the loss of a loved one. All but two of the deaths are in the playwright’s late works. Some deaths are sudden. Another 29 emotion induced deaths are mentioned as possible, but the likelihood of some can be challenged.

… My interest in this topic was aroused when, studying Hamlet, I was struck by the violence of the hero’s reaction to his encounter with his father’s ghost on the battlements of Elsinore. Hamlet’s anguished words, “Hold, hold, my heart, and you, my sinews, grow not instant old, but bear me stiffly up” (1.5.94; act, scene, line in Norton Shakespeare), seem to suggest that his heart was palpitating and his knees were buckling. The symptoms suggest a near-syncopal attack or, conceivably, a paroxysmal tachycardia causing a drop in cardiac output. — Faints, fits, and fatalities from emotion in Shakespeare’s characters: survey of the canon

Steve, you are on the wrong track here. The historical ‘facts’ you present are not verifiable. Changes in medical terminology, the lack of knowledge and skill in medical profession in previous centuries and simple misreporting, mean we have to stick to the facts that we can know with certainty.

Antony Sanderson: Good point. Everything from Dr. Kendrick gets sent to my junk folder, with the viagra ads, like several of the other high-quality blogs I subscribe to. Whoever wrote the algorithm for this ain’t the sharpest knife in the drawer. I often go straight to the junk folder first thing in the morning. That’s where most of the best stuff is located. A paranoid take on this is that it is another example of censorship.

I don’t remember where I read this claim: rodents supplemented with high doses of vitamin B6 never have strokes. Vitamin B6 is involved in the production of phospholipids, a major component of cells’ membranes.

The accumulation of oxidised cholesterol surrounding endothelial lesions may be related to a cluster of cells having serious membrane defects.

In people B6 does not seem to have any effect on CVD & stroke, whatever happens to rodents.https://ods.od.nih.gov/factsheets/VitaminB6-HealthProfessional/
“The research to date provides little evidence that supplemental amounts of vitamin B6, alone or with folic acid and vitamin B12, can help reduce the risk or severity of cardiovascular disease and stroke.”

It is pretty lengthy and most of it is how his colleagues did him in and proceeded to graft the Lipid Hypothesis on us.

The summary of Kern (as described in the book) is that blockages do not usually cause infarctions. He claims the heart has its own bypasses which could just not be modelled with too-thick glue material. KERN is claiming infarctions come from a metabolic dysregulation of the heart muscle, namely anaerobism and buildup of lactic acid. Too much of it causes lysis and too much lysis causes widespread damage aka CVD event. Points out that infarctions, unlike plaque, almost always occur in the heart, specifically in the LEFT chamber. Claims ouabaine (Strophantin) helps with the same plaque in place. Claims to have found traces of micro-infarctions, point spots in the muscle where some cells underwent dying.

They didn’t believe him, they didn’t believe Manfred von Ardenne. Every pathologist had cut his pound of calcium from the victims you see.

It certainly sounds intriguing. What I am wondering is how ouabaine is supposed to improve O2 utilization in the heart when there is no O2 in the first place? Perhaps it is not a problem of O2 perfusion in the first place, but of switching off that darn Warburg. One could perhaps reread

You know, that’s a VERY good point. I have no clue about the detailed biochemistry, but Dr William Davis’ books (and those of others) have a great deal to say about how grains – perhaps especially wheat – cause permeability of the intestinal wall. If the components that cause that pass through, perhaps they also get at arteries.

I was a member of Dr. Davis’ website for many years. I agree with his point about modern,un-sprouted wheat but not all wheat. The landmine in wheat is still the enormous amount of carbs – sprouting cleans some of those up too…

This is more a comment on what Bill said. We have to distinguish between something going through a permeable membrane and something being transported through a membrane; permeable has the implication of gaps. Indeed the blood capillaries are permeable to allow diffusion of oxgen and nurtients, that is miscellaneous stuff, that has been prepared for use. You don’t want this in the gut because there can be nastry things in there. In the gut you have transport, by the cells lining it, of specific items into the hepatic portal of the lymphatic system; this is not a passive system.
In scurvy, connective tissue breaks down due to lack of vitamin C needed for its manufacture, and then blood can leak out – an extreme example of permeability.

In this study, the importance of the glycocalyx in mechanotransduction was studied in the intact animal by: (a) investigation of the pure shear-stress response, differentiated from the acetylcholine response; and (b) investigation of whether glucose produces a differential block of the former. The reasoning for (b) was that glucose interacts with the proteoglycans (Rosenberg et al. 1997) and glycosaminoglycans (Arisaka et al. 1995) of the glycocalyx, and this may take place under hyperglycaemic conditions. There is already evidence that glucose affects glycocalyx volume (Zuurbier et al. 2005). Unfortunately, systemic hyperglycaemia involves insulin release, and insulin has complex haemodynamic effects (Baron, 1994). Therefore, the eventual experimental approach undertaken in this study was the exploration of luminal hyperglycaemia.

Errett, I tried to read this research paper. Potentially it could be useful. But frankly I could not understand it. Do they really want to be understood ? Too much gooblegook. And too much playing both sides of the argument.

It appears to say glucose prevents dilatation of the artery by possibly limiting NO release at sites with high shear stress.
“It is apparent now from multiple studies that EndotheliumCells sense and respond differently to smooth-flow and disturbed-flow.” http://atvb.ahajournals.org/content/34/11/2378

Smooth flow is high shear stress and disturbed is low shear stress. it goes on to conclude:

“The findings of this study may indicate the following theoretical mode of action: the glycocalyx gel phase determines the mechanical response of the glycocalyx, while the proteinacious ‘hairs’ within the gel, which transmit the signal to the endothelial cellular cytoskeleton, depend for correct strain (in response to change in shear stress) upon the mechanical response of the gel phase. The strain transmitted to the cell cytoskeleton could then trigger the release of calcium ions (Muller et al. 1999), or increase intracellular calcium ion concentration from sodium–calcium exchange (Tang & Li, 2004), leading to activation of endothelial nitric oxide synthase (eNOS) and increased release of nitric oxide. Relaxation of vascular smooth muscle would then seem to be just a response to nitric oxide; mechanotransduction by vascular smooth muscle itself (Osol, 1995) appears to us unlikely”

Improper dilation would be the same as stiffening the artery. It would also appear that NO is protective for thrombosis, or so I read.

Thanks Steve, yes that is what it appears to say. But there is so much back filling etc. I was doubtful. For god’s sake if you find something say it clearly ! Then we can assess what is new & worthwhile. Gobbledegook only ensures mystification.

Someone pointed out that humans are inside-out plants. Instead of us being rooted in the soil, we carry the soil around with us in our gut where our roots (villi) supply us with nourishment. And of course we breathe in oxygen and out carbon dioxide, the opposite of plants.

Dear Malcolm… could I venture a contributory ’cause’ of CVD and stroke: dehydration? The high velocity you describe of blood forced through arteries will have a shearing effect on the endothelial walls if the blood itself is thickened by the simple lack of water. This grinding and inflammatory effect will of course attract the healing LDL and build up as plaque. The very high incidence [over 50%] of stroke patients admitted to hospital with significant dehydration supports this theory.

I fully agree. I think, however, the ‘acute’ mechanism may also include greater blood viscosity and a higher level of ‘stress’ hormones released in dehydration, all of which lead to a far greater risk of thrombus formation.

Old people living alone with poor mobility cut down on their fluid intake so as not to move as much. You are so right about dehydration. Lots of ill effects from not increasing fluids, but in urgency to toilet themselves, falls become a problem. And there we get into social problems of the old and lonely, quite depressing. And of course some younger people drink questionable fluids, but is our tap water safe, no it damn well isn’t, entirely, though recently in the Llyn peninsula the water was glorious, probably from mountainous reservoirs such as Snowdon area. Such wonderful deep science Dr Kendrick, wish I was clever. Thank you.

“Our results show that all plaque sites were concomitantly subject to high LWStretch with a mean amplitude of 34.7 ± 1.6% and high LWStiff, with a mean amplitude of 442.4 ± 113.0 kPa. The LWStiff amplitude was found to be slightly greater at the plaque sites in the LM coronary (mean value, 482.2 ± 88.1 kPa) as compared to those computed in the LAD and LCx coronaries (416.3 ± 61.5 kPa and 428.7 ± 181.8 kPa, respectively). These finding suggest that local wall stiffness plays a role in the initiation of atherosclerotic lesions.” From ref 1.

It would appear areas where plaques are found have higher localized arterial wall stiffness. Stress risors could develop in these areas possibly leading to damage to cells, which would require repair. These repairs might lead to clotting action. These stresses would occur in the same places over time. Other papers list wall shear stress related to flow, however, these might be a combination of flow derived and pressure derived. The pressure derived would be increased by heart contraction stopping flow. Again happening in area where the atrial wall stiffness is increased.

Your reference 1. From that paper ref 31, 33 and 83. Any additional tensile stress, from mechanical or chemical sources (adrenalin maybe) would make this worse or a reduction in strength would also. The loads in these areas are asymmetrical and complicated. The areas with the plaques appear opposite the high shear wall stress but the plaque side is still connected to underlying heart which likely limits elasticity and increases stiffness.

Steve, I skimmed through the link you provided. In addition to ‘adaptive thickening’ that article mentions something else important (on page 129 ? ) “Collagen plays a role in the attachment of endo- thelial cells to the subendothelial matrix, thus con- tributing to endothelial cell integrity.

I have mentioned Dr Lester Morrison time & time again here for his experiments with Chondroitin sulfate to prevent ‘heart incidents’ in the 1960 & 70’s. And Seneff has had articles published about the importance of sulfates in helping to ensure the integrity of the endothellium layer of cells within the arteries..

But why was Chondroitin Sulfate the form which Morrison had such success with ? Would not some other sulfate source work as well ?

I think the Stary, Blankenhorn, Chandler, et al paper from 1981, offers a coherent substantial reason why CS is so effective. The attachment of the endotheial cell lining the arteries is achieved with collagen. But as we age the body looses the capacity to generate all the various types ( 5 if I read this article correctly ) of collagen needed for this process.

Chondroitin Sulfate is in fact composed of collagen and I suspect contains all 5 different types of collagen needed. Hence it is effective at helping heal CVD, as discovered by Morrison in 1973

Bill in Oz: For about six years I have been making and consuming (1 cup/day) bone broth. I hope this has all five types of collagen. I make it from, among other bones, the knuckle joints and feet of the cow. It gels like jello if I put it in the fridge. Plus now I’m taking the GS/CS daily.

Rob, that’s an interesting article from 2011. In the discussion there is this statement :
“The initiation, development, and progression of atherosclerotic plaques in vivo is a highly complex process, modulated by systemic risk factors but also triggered locally by the interplay of mechanical factors as local stress, strain, stiffness, and arterial wall remodeling, which contribute to the distribution map of atherosclerotic lesions along the arterial tree. Our findings may provide better insights to understand the mechanisms triggering the initiation of atherosclerotic lesions. ”

This is fascinating. Excellent find.
“Remarkably, such zones of high stiffness concentration correlate with clinically identified lesion sites (Fig. 6C). Moreover, our results show that, in all studied cases, the stress and LWStiff maps have similar spatial distributions. In other words, sites with high LWStiff were also found to be sites with high stress. Similarly, sites with low LWStiff were found to have low stress (Supplemental Fig. S1).1”
It appears that the heart contractions add to stress increases. Likely why the lesions only occur here. According the ref I listed above the areas identified as high stress respond by adding muscle and other cells as well. That paper also states the cells are not the same as typical smooth cell muscle. Maybe that’s why the EC responds differently. Different substrate. This is headed way past me now into cell adhesion and chemical signaling. Doc and others your turn.

As a layperson, the idea of pressure, speed and confluence points/junctions makes sense. But it can’t just be that or else we would all be dropping dead at all ages in large numbers. Evolution can’t have been that short sighted? All things being equal, the body of a 10 year old has to be in better shape than a 70 year old.

Surely we have to factor in poor diet, bad lifestyle (e.g. sedentary, smoking) and the general debilitation of the body over time as we age and weaken as adding to the susceptibility of the constantly under pressure arteries to sustain damage.

Charles, I have printed off the Seneff article to read at my leisure. There is much that I like in it. but also some that is perplexing. An initial comment : I am a bit doubtful about the strength of her linking of CVD with glyphosphate. There may be a link but I doubt it is the major ’cause’.

Why ? Because my own personal work life contradicts it. I have been an organic farmer since 1986. I have used Roundup maybe 5 times in the 32 year period since. And never on soil which I was using for crops or vegetables. Also I have mostly preferred organic foods over conventional foods. So my contact with the herbicide has been minimal I suggest. Yet I have CVD and a high Calcium score in one artery.
One further thought : If Seneff is correct then CVD rates should be extremely high among farmers using lots of Roundup on their crops or farms. Eg. Grains & seed oil farmers using “No Till’ methods of farming. No Till has become extremely common among conventional farmers in Australia, the USA, Canada etc. since the introduction of crops engineered to tolerate Roundup about 20 years ago.

So I wonder is there any epidemiological evidence supporting this ? It may exist but have not seen any. Or maybe it is emerging.

Bill in Oz: Monsanto has worked tirelessly to stifle research into glyphosate, and viciously attacked any and all disagreeable findings. California just added glyphosate to its list of probable (possible, known? not certain what the legal; terminology is) carcinogens, which require labelling. Monsanto sued to stop this, and lost. There is some justice in this world.

Gary I suggest it would still be extremely easy to access CVD & heart disease death statistics in districts where a lot of Glyphosate is used in grain & canola farming districts. Such information is usually public access.

Bill in Oz: The evidence I have seen about the toxic effects of glyphosate is mainly biological, rather than epidemiological. This, too, would be difficult to come by, as its use is so widespread in homes and gardens now, and because Monsanto owns the U.S. government, who refuses to do after-market monitoring of it, or even testing of the food supply, just as they fail to do with vaccines. No after-market surveillance of any value. Down there you folks have it worse on this score than we do.

Gar in the 1970’s i lived in East Gippsland, in Victoria, Australia, near a town with a big horticulture industry. It was standard practice to spray the weeds in these vegetable growing areas with such sprays as 24D etc.
And this same area in a few years showed up as having a large cluster of severely intellectually handicapped children and physically handicapped kids as well. The link was never proved. But the farmers wives spread the word and exerted ‘moral’ pressure on their husbands, to change their sprays. And gradually the population statistics ‘ normalised’.

The people of that area also became far more interested in organic growing. That town is now the home base for one of the major organic associations in Australia – the OAAA.

As for the no-till, glyphosate ( Roundup ) farming methodology, it came here from the USA & Canada. It is a good reason to stay away from canola and conventional grains and the processed foods they are ingredients used in – such as bread, cakes, breakfast cereals, industrial oils.

One thing I still can’t quite get over is the epidemiology of cholesterol. Those (I should say men between 35 and 59 yrs) who have cholesterol above – say 230 mg/dl – have a higher rate of both overall death and cardiovascular disease death. Yes, yes, I know that this is just a correlation, but it is indeed a compelling one. Too, the taking of statins does lead to a decrease in cardiovascular endpoints relative to a placebo. Perhaps this has nothing to do with cholesterol lowering (the dreaded pleiotropic effects), but it too is compelling. In most primary prevention trials this does not lead to a decrease in overall mortality in the statin group, but cardiovascular death does decrease in the statin arm. (I can picture a doctor talking to the wife of a patient. Doctor: “I have good news and bad news.” Wife: “Oh dear, what is it.” Doctor: “The bad news is that your husband has died.” Wife: “That is awful.” Doctor: “The good news is that he didn’t die of a heart attack.”)

It seems to me that the presence of cholesterol in the plaque indicates a role for cholesterol in the pathology of cardiovascular disease. I believe it is overhyped to sell statins and cholesterol testing and to keep the gravy train of money coming for cholesterol research, but I believe there is a small role, and if there is a role, it is plausible that it is concentration dependent.

25-30% of our brain is made of cholesterol, would you associate brain diseases and cholesterol and say it’s a compelling correlation? Also, memory loss is one of the side effects of cholesterol-lowering drugs. The truth is cholesterol is everywhere in our body and it’s crucial, so crucial that without it we die.

Every cell in the human body got cholesterol, it’s part of the cell membrane.

So if we look up at injuries, it’s normal to find cholesterol. Cells use cholesterol to “talk” to other cells, so it’s perfectly normal that they talk to each others and say let’s repair this injury (arterial wall damage for example) The adrenals and sex gland produce steroid hormones, and i think these hormones are used for tissue reparation. My take is, everytime there is an injury in the body, cholesterol in this area should be found in higher concentration, and that would be logical. Why? because cholesterol is needed in the production of hormones. (testosterone, progesterone, pregnenolone, androsterone, estrone, estradiol, corticosterone, aldosterone etc.)

I love this quote from Voltaire:
“The art of medicine consists in amusing the patient while nature cures the disease.”

A side note : I do wish that there was one standard global method of measuring cholesetrol. Here in Oz and in New Zealand and I gather in the UK, medicine uses mnols while in the USA it is mg/dl.. And maybe Europe, Asia and Latin America etc have other different measuring methods.

I suspect that a lot of the confusion in understanding CVD could be because there is confusion as a result of these different measuring systems.

So if all the extreme stress in the coronary arteries *may* cause problems, why is exercise, particularly vigorous exercise an unequivocal good? Surely this would increase the stress etc and thus cause more problems? Just a thought and probably not a good one; it’s the end of a very long day….. Great article though.

Perhaps it does unless anyone can show that people who exercise in great amounts eg tri athletes and the like, live longer than average. I suspect they do not but would be happy to be shown evidence to the contrary.

Surely exercise will follow the same ‘J’ curve as many other things that affect the body. Too little isn’t good, but it is possible to take too much. Think of alcohol, or salt, or even water. I’d guess tri- athletes are probably overdoing it. I know one man who ran so many marathons, he now has severe arthritis – so probably he gets too little exercise now.

The only reason for my own MI survival 1999 were (as I was told), and still are, the collaterals around all my blocked arteries.

I have though never seen any good explanation for how these collaterals develop other than that it must be a very good homeostatic repair logic for this “naturally” occurring by-passing with micro-vessels.

Dr. Göran Sjöberg: I recall reading from one of the previous posts a commenter linked to how the collaterals develop, and as I recall, they develop in response to the restriction of flow as atherosclerosis progresses, narrowing the diameter of the lumen.

Tremendous article! I’m the 71 year old with LDL over 500mg/dl and plaque-free arteries. A lipid researcher at Harvard told me, in a lengthy telephone conversation, that the reason I don’t have plaque is that I obviously have a protective mechanism that counteracts the “obviously damaging effect of my extreme lipid profile”. He most emphatically denied my hypothesis that I simply did not have some unidentified mechanism that causes plaque to form. Nope. Couldn’t be as simple as that. I countered that it seemed strange that evolution would provide someone with FH (me) with such a powerful protectant that I’d have no plaque even with an extreme amount of “bad” cholesterol, but he was adamant. A second medical expert recognized the improbability of a rare “special protection” being available for a rare condition, so told me that the “protection” I have against plaque is probably present in many normal people also, What?! So now there is a protection lurking amongst all of us that protects people of all lipid levels. (I.e., lipid levels don’t matter but the protective mechanism does?)
Your explanation, of robust endothelial cells, is such a succinct concept and would so perfectly explain why neither I, my FH older sister or our FH mother never had any coronary issues at all.

Total cholesterol (presumably with typically high LDL) above 300mg/dl since at least 1966 (age 20), even with all the available lipid lowering treatments (ultimately including statins) hardly ever below 300. Then, maybe fifteen years ago (guesstimate) after finding by EBCT that my arteries were clear, I quit all lipid lowering efforts. Since that time my total has been both sides of 600 mg/dl and my LDL has been both sides of 500. I had five EBCTs over about ten years and three scores were zero and two showed extremely small amounts of calcium (described as totally trivial by the cardiologist). My last score was again zero.

Thanks Robert for your comment. And being willing to share some of your own & your family’s personal health info.

It illustrates again the faith based nature of the whole cholesterol ‘disease’. Some people still believe in fairies at the bottom of the garden. Such folk are less dangerous and far less frequently so arrogant.

And LDL of 13mmol/l (500mg/dl) is pretty much as the upper end of anything. You have become victim of what Karl Popper would call, circular logic.

Consider the following dialogue:

Person A: ‘Why is the sea so rough today.’
Person B: ‘Because Neptune is angry’
Person A: ‘By what evidence can you support your statement that Neptune is angry.?’
Person B: ‘Oh don’t you see how very rough the sea is, and is it not always rough when Neptune is angry.’
Popper K: Selections

Changing this over:

You: ‘Why do I have no heart disease when my LDL level is so high?’
A Cardiologist: ‘Because you are protected.’
You:’ ‘By what evidence can you support your statement that I am protected?’
A Cardiologist: ‘Well, look at how high your LDL level is, and you have no heart disease, so you must be protected.’

Goulboy
This article opens up by stating that LDL-C penetration of the artery has been “demonstrated”. In the conclusion it then lists 5-6 sources to support this statement.
Here is source 1 from 1976
Atherosclerosis. 1976 Jul-Aug;24(1-2):99-106.
Effect of hypertension on the entry of 125 I-labelled low density lipoprotein into the aortic intima in normal-fed rabbits. Bretherton KN, Day AJ, Skinner SL.
“The results suggest that hypertension in the normal fed rabbit increases lipoprotein entry into the arterial wall by an effect on vessel wall permeability rather than by a direct effect of filtration pressure. ”
In other words the artery endothelium is damaged by hypertension and then lipoproteins can then enter the arterial intima.
However Goulboy your link asserts that this source proves it is the other way around. That is poor science.

Goutboy, moving on, the abstract of second source cited by your link to ‘demonstrate’ that LDL-C causes CVD, states again for rabbits )
” At 160 mmHg, CLDL and C.Ib were markedly increased” in the arterial wall of rabbits.
NB : Again it is hypertension which CAUSES the damage to the rabbits arterial endothelium and allows LDL-C to penetrate.

The third source listed is ” Structural Changes in Rat Aortic Intima Due to Transmural Pressure by Y. Huang, K.-M. Jan, D. Rumschitzki and S. Weinbaum from 1997.
This research was done on rat arteries. The abstract of this is not clearly written. It is mostly about pressurising rat arteries. It does not seem to offer any view on LDL-C causing CVD by penetrating coronary artery endothelium. The article is also paywalled despite being 20 years old.

Goutboy, turning to N Karmakar’s article cited as the third souce from
Atherosclerosis. 2001 Jun;156(2):321-7. : Interaction of transmural pressure and shear stress in the transport of albumin across the rabbit aortic wall.”

Here is what the abstract of the 4th source cited by your link, actually states
“The net outcome arises as a result of the interaction of increased permeability of endothelial cells exposed to shear stress, the pressure induced distension of the wall matrix and the differential effect of EDRF/NO at the two pressures on medial hydraulic conductivity.”
In it’s rather obscure way this actually supports Dr Kendrick’s hypothesis that hypertension and shear stress is the key to CVD. Damaged endothelium cells allow lots of stuff from the blood stream to enter the artery wall. Yes that’s what we would expect surely. The abstract does not discuss LDL-C as a causal factor or demonstrate that it is a causal factor,.

It is “Effects of Pressure-Induced Stretch and Convection on Low-Density Lipoprotein and Albumin Uptake in the Rabbit Aortic Wall ” by Guy Meyer, Regine Merval, Alain Tedgui from “Circulation Research”.

It is open accessed from 1996. This research was done on were done, once again rabbit arteries – not humans. There is in the article this paragraph :
” In order to evaluate the role of the endothelium, an additional series of experiments was conducted under similar conditions using vessels excised as described above. After cannulation, the endothelium was stripped from the luminal surface by gently passing a 4-mm-diameter balloon catheter through the cannula into the lumen of the vessel. We have previously shown that by use of this method, the endothelium was completely removed and that an intact elastic lamina and a normal underlying tissue were maintained with viable smooth muscle cells.”

In other words in order to assess how permeable rabbit arteries are to LDL-C, they removed the endothelial layer – which is the layer of the artery which makes it usually impermeable. This is utterly bloody stupid research.

And does not provide any evidence to support the hypothesis that LDL-C causes CVD.

But it does perhaps provide us with some insight as to why balloon angioplasty and stents fail so often after a year or so. The process strips away the endothellium layer of the artery which is essential to long term arterial health.

Goutboy, the 6th source cited by : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2755980/ is the following from 1984 in the Am J Physiol.
“Filtration through damaged and undamaged rabbit thoracic aorta.” by A Tedgui & MJ Lever. Again it is research done on dead rabbit arteries which have the endothellium layer removed.
In the Abstract is this sentence “Removal of the endothelium can increase the hydration and porosity of the medial interstitium ”
Yes it can. But it tells us absolutely bloody nothing about what happens in the arteries of living human who have not had the endothellium layer removed.

To cite this as a source supporting the hypothesis that LDL-C causes CVD in humans by penetrating the arterial wall, is fraudulent medical research.

Goutboy, here is the 7th and final source cited in the first sentence of the discussion section , by https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2755980/
The source is the journal Hypertension from 1990 – 27 years ago.
“Transendothelial macromolecular transport in the aorta of spontaneously hypertensive rats.”
The authors are :Wu CH1, Chi JC, Jerng JS, Lin SJ, Jan KM, Wang DL, Chien S.
Again arteries from dead rabbits were used in this research.
In the abstract can be found this statement :”The number of leaky foci per unit endothelial surface area in spontaneously hypertensive rats was found to be approximately three times that in Wistar-Kyoto control rats; the frequencies of both endothelial cell mitosis and death in spontaneously hypertensive rats were also approximately three times the corresponding values in Wistar-Kyoto rats. These findings indicate that hypertension in spontaneously hypertensive rats is accompanied by increased endothelial cell turnover and an attendant enhancement of permeability to macromolecules.”

Some final general thoughts on the article you linked to Goutboy
1 in a sense this is a ‘good find’ as it shows up how medical research can mislead.
2 : It tool me some hours to go through the 7 sources cited and work out for each source whether it was being cited correctly or incorrectly. And I suspect that the authors relied on this, to assert what they did. They rely on reviewers. editors & readers not going & thoroughly checking their cited sources.
So I suggest that we here commenting on this blog should check out the articles and links we offer here. It will save us from being misinformed and distracted.
3 : Some may ask what the significance of all the mathematics used in this research paper. And frankly I have no idea. It may be hocus pocus. It may be worthy some thought. But it is not apparent to me that it offers any clear methods of curing, healing CVD. And that after all is supposedly the point of this medical research. But I admit I may be being harsh on this point.

Yes. Just try to find a definitive statement e.g. LDL can, or cannot be transported though an undamaged endothelial layer. This is impossible. Or at least I have found it impossible. When this happens, I now know that something is being ‘hidden.’

Anthony, I seem to have gone into an attack mode the past 2 days. I grew angry at fraud being presented as reputable medical science. As I progressed in examining the 7 sources that supposedly ‘demonstrated’ that LDL-C causes CVD, I was amazed at the extent of the blatant misinformation turning up.
It was even ‘hidden’ as such. It was sitting out in the open waiting to be ‘pointed’ at. I feel a little like the small boy is the story of the emperor’s new clothes.

And now Prof. Ray et al. have published their study about prevastatin.. My comments about i the books being cooked, ( especially re the placebo group ) are already in this blog. And again, I feel like the boy pointing out the lack of clothes on the emperor.

Another enjoyable and fascinating read (actually 3 reads – the first on the screen doesn’t really count, but a couple of reads of a printed version). My approach is “what does not cause heart disease” and I’m sticking my neck out by eating real food, exercising every day (easy with a dog & a bike ride to/from work) and getting out at work at lunchtime (& in the sun when shining). [Though need to work on the not drinking too much at the weekends.]

In terms of the conclusion, I love the ‘And it can’t, so it is’. The cholesterol hypothesis was dead for me as soon as I started reading into it and am more than happy to learn about more nails in the coffin.

I feel sorry for your recycling bin after having been stuffed with 20,000 torn papers. What this serves to highlight though is the incredible amount of bulldust being published – often in peer reviewed publications. Most papers merely generate hypotheses or show associations of varying degrees. Few actually prove anything beyond reasonable doubt. Many simply assert things that aren’t true. Perhaps my own quest for certainty is a goal too lofty. Perhaps I shall have to accept phrases like ‘x can lead to y’. What I can say is how much I appreciate reading this blog and other publications produced by Dr K. No bulldust here! Tis why I keep coming back.

Antony Sanderson – no there’s nothing in my spam or junk folder. It’s very odd because it’s only in the past month or so I have stopped getting notification of comments. I always got notified by email, now I need to check the blog to see ‘what’s occurring’. I’ll still tick the boxes – it may suddenly start to work for no apparent reason, as I have found before with technology!

Thank you so much for this, Dr. Kendrick. Upon the second reading I took notes. I now understand how the BBB operates. Tough little critters, endothelial cells, and versatile. Trying not to think about my coronary arteries getting smashed flat all the time. Ouch!

If they ever find a way to expel you from your job for telling the truth, I think you could start writing a wonderful range of down to earth medical textbooks – because excessive jargon just clogs the mind up. Any profession that can name a disease “Bovine spongiform encephalopathy” rather than “Mad Cow Disease” needs to consider its priorities. BSE made me realise that a medical sounding name could obscure the fact that (at the time) nobody knew anything significant about this disease.

I never knew that large blood vessels needed their own small vessels to service them – though I suppose it is obvious now I think about it. I picture a tree trunk with ivy growing up it.

I also didn’t know that the brain makes its own cholesterol – which raises two obvious questions:

1) Does it use the same synthetic route and same enzymes as the liver?

2) Can statins (or at least some types of statins) cross the BBB?

I wonder if the vasa vasorum sometimes get blocked – thus starting the damage to the epithelium (by starvation), which causes the plaque, which ultimately breaks off and blocks a larger vessel …..

This bugs me: Hillary Clinton has a ZERO CAC and she must have lived under enormous stress and eaten a boat load of carbs! I am tiny, not so stressful life, age 57 CAC score 70! Trump is 50 CAC. Go figure! It can not be just the carbs and insulin and stress…. that eliminates a whole lot of conjecture for me…. the mechanism is out there, we just have to find it….

Mono, Jon, Jon K
I have never used warferin. Thanks for the tip ! As for Hilary, ‘Hils’ as she would quickly become named here, she should be trying low dose aspirin. It’s very effective as an anti coagulant without the arterial calcification side effect. Just have to be careful to check for hidden bleeding in the gut.

Hi Bill in Oz am Shannon in OZ… thanks for reply, I am at a loss to explain too! All I think of is I ate Veg oil and Low card diet as per Govt guidelines my entire life…. don’t drink that much , exercise etc etc … anyway, it is what it is, I have lowered insulin greatly as per 2 hour insulin test , my CRP is lower since I cut carbs under 50 g a day too… we shall see, I would rather pop off with heart attack than cancer, is that a bright side???

Lovely, Dr MK, you have given me lots to work on. The arguments are just what I like to use myself. Although not fool-proof, these were what struck me about cholesterol and saturated fat – if they are so bad for us, why after millennia of evolution do we make so much of them?
On the flow in pipes, I think there are some misconceptions in the comments. Blood from the aorta does not flow through an ever narrowing pipe, but into a splitting multiplicity of narrow pipes, so you cannot make simple assumptions about velocity especially as the pipes are in a moving, elastic medium, which will also contribute to the flow. It is not like the flow of a liquid in a rigid pipe with diameter much bigger than the molecules of the liquid. In the fine capillaries the erythrocytes will be travelling singly separated by blobs of plasma.

Doctor Malcolm:
“Another place of extreme biomechanical stress is within the coronary arteries. These arteries are exposed to a unique stress, in that they are compressed with great force when the heart contracts. Some have likened this to stomping on a hose every second.”

• Is it not true that plaque forms in the larger coronary arteries that rope around the exterior of the heart?
• Is it not also true that only the smaller coronary arteries and arterioles that actually delve into the muscle of the heart are the ones that get flattened by its contraction? (The flow into the myocardium only occurs during diastole, yes?)
• And, is it not true that those inward delving vessels have less plaque – if any?

SW: Seems to me to be another symptom, another correlation. I had an annoying shoulder problem a few years ago in the shoulder which lifts dishes into a high cupboard. Doctor sent me to one of those claustrophobic tubes, and found some minor rotator cuff tears. This has not recurred since I’ve been doing strength training.

Dr Malcolm,
You described to us a while ago how a clot is formed at the site of a stripped away endothelial cell(s) due to the Tissue Factor that’s released by the underlying exposed tissue initiating the coagulation cascade.
Arterioles can generate TS, no?
Is it that arterioles are simply too small to generate the turbulence and stresses that damage? But what does that have to do with considering Tissue Factor?
(I generated a tissue factor/arteriole search on pubmed and found one article on pulmonary arterioles in rats. ??)

Dr. Kendrick—–I have been exploring nanomaterials and their impact on our health—-we seem to be swimming in a sea of nanoparticles that can cause havoc in our vasculature system—-one more factor we may need to incorporate into the analysis of CVD—–

Endothelial cells lining the lumen of blood vessels
serve as a physiological barrier that controls
nanoparticle transfer from the vasculature into the
tissue. Indeed, endothelium is particularly important
in controlling the passage of macromolecules and
fluid between the blood and interstitial space. The
loss of this function is a result of tissue
inflammation. Thus, the efficient transfer of many
water insoluble substances from the blood into the
interstitium relies on endothelial permeability, and
often requires specific carrier proteins [58]. Nanoparticles
may induce endothelial system inflammation
and subsequent dysfunction either by escaping from
phagocytosis and interacting directly with the
endothelial monolayer or the nanoparticles may be
phagocytized by monocytes and provoke oxidative
stress responses [117].

Dr. Kendrick,
I have a question. If ” The metabolism of brain cholesterol differs markedly from that of other tissues. Brain cholesterol is primarily derived by de novo synthesis and the blood brain barrier prevents the uptake of lipoprotein cholesterol from the circulation” – then does this mean that the brain is not starved of cholesterol by taking statins? I had thought that perhaps a reason that statins increase dementia was because the brain gets starved of cholesterol.

Oh…but isn’t the mechanism of action in the liver anyway? I mean, my question was, if the brain makes its own cholesterol, then the brain should not be deprived of it even if the person takes a statin…?

I saw this in the Guardian. No research paper cited at all. So who’s to know how accurate it is. A Google revealed 6 other reports all based on the Guardian’s report. It seems that the author Professor Ray is doing some self promotion here.

Goutboy, I shall do that. But first I am working through the wave of comments here, seeing what others here have to say. The most significant one is the issue of absolute risk & relative risk. ( Sorry I forget by whom just now ) And I suspect that Dr K will have some interesting thoughts also when he has teased it all apart..
But right now it’s earlyish Friday morning here in Oz , after a late night out dancing. ! So a shower & breakfast & a pot of tea, are the order of the day. 🙂

Average cholesterol level in WOSCOPS was 7.0mmol/l. 44% were smokers, 10% had pre-existing CHD and the rate of CHD in Glasgow when this study began was five times the current UK average. So, clearly, this population accurately represents the average UK citizen.

And, according to Kauffman, the NNT in WOSCOPS was 500. A bit underwhelming. Interesting that in both EXCEL and AFCAPS the treatment group had worse outcomes than the controls! Do the statinators mention these trials? Ha.

Circulation. DOI:10.1161/CIRCULATIONAHA.117.027966 but : This study was partly funded by a grant from Sanofi to Imperial College London. The WOSCOPS trial was originally funded by Bristol-Myers Squibb and Sankyo.

This newspaper exposure of 28%, unqualified by details, without access to the research details seems fundamentally wrong to me. I looked at lead researcher Kausik Ray’s publications list where he is lead author and found no mention, but he has done work showing that LDL is lowered by statins. Is this research just another one of – statins reduce LDLc and therefore reduce CVD risk?

Thanks for this. It will take a while to work through, but Dr MK has probably already made the most relevant comment above. The cynical comment on the unreferenced newspaper reports would be that they wanted to get the spin out before the critical analysis could catch up.

My first comment on Ray’s effort published in Circulation today
1: It is an observational followup at 20 years of the original WOSCOP 5 year trial, based on the statistics provided by Scottish health authorities.

There seems to have been no individual interview followup of persons in either the trail group or the placebo group.

2 : I have just read this ” at 5 years after the initial trial finished approximately one third of individuals originally allocated to pravastatin or placebo were on statins.”

Duhhhh ? What does this mean ? I suspect it means that a whole lot of Scottish men originally in the placebo group were put on statins as well…This is a weird confounder !!

I suggest that this confounds the published results & claims.

But I will think about it more today.

Probably will be delayed in followups: my lady wants a holiday break day away from study, home and work

I have looked more at page 5 of the research paper. And I wonder if the ‘books’ have been cooked ?

Why ?
In 1997 ( 20 years ago ) this trial started off as the WOSCOPs trial
(i) 6595 individuals in the trial
(ii) All men
(iii) All had no evidence of MI or CVD
(iV) All had LDL-C equal or less than 155 mg/dl
(v) Nobody with LDL-C more than 232 mg/dl was allowed in the trial.
(vII) The 6995 were assigned to one of 2 groups : treatment or placebo of roughly equal size
(Viii) ssesment to placebo or to treatment group was random & was blinded

ANALYSIS : There was No selection criteria to exclude smokers – as smoking causes MI & CVD independent;y of anything else. Dr K says that 10% of the 6595 (= ~ 590 ) were smokers. This is a major confounder.
There is no information if ( by chance) many more smokers were assigned to the placebo group than the treatment group. Professor Ray needs to provide the numbers if he wants credibility.
This is also a possible major confounder

I think we need also to seriously analyse the nature of the Placebo group. I cannot find the exact number in the placebo group. But I assume ~ 3500. These men were getting no prevastatin but were aging and as they aged, it is highly likely that their LDL-C blood levels were rising. It is a common characteristic of the age group in our modern societies.
And in the UK these men were also being treated by GP’s as part of the NHS. Any man in this group presenting to a GP and having a high LDL-C, would as a matter of normal practice in the late 1990’s – 2100’s been offered a statin prescription by their GP. After all the GP did not know & the patient did not know if a man was getting another prevastatin.
EFFECTIVELY (i) THERE WAS NO PLACEBO GROUP FOR THIS TRIAL. AND SO (ii) COMPARING THE PLACEBO WITH THE TREATMENT GROUP IS PRETTY MEANINGLESS.

Finally I suspect that the books were cooked in another way. Professor Ray states on page 5, that at some point, 1066 of the original 6995 men were excluded from the 20 year followup analysis,
” if there was evidence of angina,intermittent claudifiation, stroke, TIA, or minor ECG abnormalities”
However Ray does not state when this exclusion took place. Was it after 5 years in 2002 or after 20 years in 2017 ? Nor does he state how many of the men excluded were from each arm of the study.
I suggest that these men with ‘heart issues’ who were excluded, should have been included so independent observers could check this out.

Bill,
It might be even worse. We know that a high proportion of people stop taking statins (about 70% after four years, from memory), so it is entirely possible that after five years when they were no longer tightly monitored, the statin group chucked their pills in the dustbin. Meanwhile the placebo group were put on statins by their GPs acting on NHS mandate. So in fact the statin and placebo groups had totally switched and in fact the data proves that statins give you 28% more heart attacks.

Martin, you are right to wonder about this. Last night before sleeping I was wondering exactly the same issue.
There are some assumptions in Ray’s research paper :
1 : that all the men in the treatment group kept taking the pills -‘were compliant’ for 5 years, even though the men did not know if the pills were an actual drug or a placebo.
2 : That the placebo group were not prescribed statins by their NHS general practioners to reduce LDL-C during the 5 years.

The same issues are even more important for the 15 year long ‘observational’ followup. There is nothing in Ray’s paper which informs us of what the men did during this 15 years which could/would have affected LDL-C levels.
Again I suggest that if these men had developed high LDL-C levels in the course of going to their GP’s, it’s highly likely that they would be prescribed some statin or other.
A personal note : I discovered recently that my younger brother was somehow prescribed 7 took, 2 different statins over a 10 year period. I wonder is this ‘normal’ or a medical ‘stuff up’ ? And did it happen to some of the men in this WOSCOP’s study ?

30% dropped out ! Thank you. So that’s ~ 2098 out of the original 6995 men selected to take part in WOSCOPS. So at the end of the trail with Prevastatin roughly 4897 were ‘compliant’.
A couple of questions Dr K.
How many of the treatment group dropped out ? And how many of the placebo group dropped out ?
I read that roughly 1100 men from the total were taking statins apart from prevastatin, at the end of the 5 year trial period. Were these ~1100 in addition to the 30% who were ‘not compliant’ or separate from them ? If they are in addition, the number of men complying at the end in both groups would have been greatly reduced – around 3700.

It is fair to assume that Ray’s observational conclusions 15 years after the trial was finished, are based on 3700 ? As the actual number becomes smaller so the potential for randomness in the outcomes between the 2 groups, increases.

And at the back of my mind is the thought “What medical treatment did these men receive in the intervening 15 years ?”

Ray makes the assumption that the ( small) differences in outcomes between was entirely due entirely to prevastatin taken for 5 years 1997-2002.

I like the photo at the top – erythrocytes struggling to get past those fatty lumps – clearly saturated fat & cholesterol. But there is some honesty, “statins reduce the risk of death in this specific group of people” – not everyone.

Martin
The concluding statement of the trial estimates that if 1000 men with hypercholesterolemia take statins there will be 9 fewer all cause deaths – .09%, which is ‘slightly’ less than the claimed reduction of over 20%.

But, at bifurcations this neat pattern must break down, for two reasons:
— Being turbulent, the streamlines are unstable, so in which direction do the elongated cells line up?
— When pointy cells aligned in two different directions meet up, they can’t mesh together perfectly. They either have to leave large irregular gaps, or misshapen endothelial cells have to grow to fill in the gaps.

Either way, it seems bifurcations must be a weak spot in the endothelial sheath, leading to enhanced chances of plaque formation.

Martin, in the midst of looking at the new ‘research’ paper by Prof Ray, and thinking it through, I almost missed your comment here, about endothellium cells being ‘streamlined and aligned with the blood flow to deal with the rapid current..’

Now this is important and the pdf you gave the link to ( from 1981 ) is a very useful source for better understanding of the causes of coronary heart disease. Thank you.

Interesting. Just thinking, I would not expect turbulent flow at branches under normal conditions just lower wall shear stress on the outside walls. The normal artery will dilate when exposed to high wall shear stress which decreases the velocity and thus lowers Reynolds number. Also the flow is pulsate which appears to have a higher critical Reynolds number. If the dilation mechanism does not work properly maybe then we see negative wall shear stress or flow reversals. This would also increase wall tensile stress and increase smooth muscle/collagen in response further limiting diameter and possibly elasticity. Maybe all this leads to EC damage and starts the process.https://eprints.soton.ac.uk/46209/1/bank_07.pdfhttps://www.hindawi.com/journals/cmmm/2015/515613/http://www.mcs.anl.gov/~fischer/pubhtml/high_re.pdf

Simplified they say it takes a really big blockage to get turbulent flow and then it is mildly so. I was looking for a reason to mechanically damage endothelium and why do lesion happen here. When blockages do occur the flow change may be why they blow apart. The papers listed in a thread above indicate higher tensile stress regions correspond to high wall stiffness and cell matter is added there to offset the loading. This is something different than other artery wall locations and is probably the where and part of how. Still need a change in endothelium to get to exposure of cells that lead to clotting. Other papers seem to indicate endothelium releases different enzymes in different flow regions and when in contact with different cells and hormones/enzymes/proteins may change the way this same cell responds. There is likely a number of different reasons for the same end result. If you identify some these then you can protect the vulnerable area. Until just guessing. The question is does the endothelium get damaged in this area first/only or does wide spread damage only effect artery wall in the high stress area?

I managed to find a well-hidden copy of today’s article [try http://circ.ahajournals.org%5D. It states unequivocally that statins cut deaths by 28% over 20 years, solely by reducing levels of LDL cholesterol. It fails to mention that 45% of the participants were also current smokers. The latest ONS statistics state that the level of smokers in the UK had fallen in 2016 to 15.8% of the adult population. All of the participants in the study were from the West of Scotland [my own background].

It is possible that statins did have a beneficial effect, but not simply by reducing ‘bad’ cholesterol. As we all know now, statins – like healthy diets – have the beneficial side-effect of lowering cardiovascular inflammation provoked by habits such as smoking. Neither the press release nor the detailed study considers this possibility, so obsessed are they with blaming high LDL levels.

Nice find, Gordon. When I’d seen the, ahem, article, I couldn’t help but laugh when I read this –

“Senior author Professor Kausik Ray, from Imperial’s School of Public Health, said: “For the first time, we show that statins reduce the risk of death in this specific group of people who appear largely healthy except for very high LDL levels.”

Largely healthy except for the smoking bit. No suggestion that the raised LDL might be a marker for other health issues as opposed to an issue in and of itself.

Gordon, my GP suggested statins for my 7.2 cholesterol result . Discussed my HDL(good), TG (good). Gave GP a 2 page report of why I am refusing statin therapy, benefits of HFLC and adverse effects of statins.
Bottom line: LDL-C is not a factor if LDL particles are healthy ie not small and dense. Ratio TG/HDL < 2 is a good indicator of healthy LDL

biddy 99, my 2 page reason for declining statin use. (Subject to change if new information emerges). References available but not listed if GP wants to discuss any item.
Diet vs Statins

HIGH FAT – ADEQUATE PROTEIN (60-100g) – LOW CARBOHYDRATE ( diabetes

STATINS
LDL-C is not a risk factor for CVD, glycated oxidized sdLDL is.
“statins reduced the potential of mesenchymal stem cells (MSCs) to differentiate into macrophages while they exhibited no direct effect on macrophage function. These findings suggest that the limited capacity of MSCs to differentiate into macrophages could possibly result in decreased macrophage density within the arterial plaque, reduced inflammation, and subsequently enhance plaque stability.”
“Statins also impaired the expression of DNA repair genes”
“statins impaired the osteogenic and chondrogenic differentiation potential of MSCs and increased cell senescence and apoptosis, as indicated by upregulation of p16, p53 and Caspase 3, 8, and 9.”
Coenzyme Q10 depletion > reduced mitochondrial ATP production
Statins disrupt the mevalonate pathway, affecting function of every one of 50-75 trillion cells and tissues in the body resulting in many adverse effects.
Expert Rev Clin Pharmacol. 2015 Mar;8(2):189-99. doi: 10.1586/17512433.2015.1011125. Epub 2015 Feb 6. Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms.
Statins are a mitochondrial poison. “Mitochondrial damage in the heart is a downward slope to cardiomyopathy or heart failure.”
Statins disrupt blood glucose metabolism and promote diabetes
Statin interference of vitamin K2 production promotes soft tissue calcification and abnormal bone and cartilage mineralization
Statin use associated with increased odds of having a back disorder, including spondylosis, intervertebral disc disorders, herniated discs, and spinal stenosis
Recent study demonstrates that treatment with statins appear to negatively affect tendon cells and extracellular matrix. The biomechanical properties were decreased and the gene expression patterns were switched to a catabolic profile.
A growing body of literature suggests that statins, in addition to being direct myotoxic agents, may also promote, unmask, or potentiate an underlying autoimmune myopathy, including a newly recognized autoimmune-necrotizing myopathy [28•, 29•], dermatomyositis, and polymyositis, in which these diagnoses are supported by histologic findings, often in combination with specific associated autoantibodies. Increasing evidence also indicates that apoptosis is involved in autoimmunity, possibly because of impaired clearance of apoptotic cells, which may in turn incite an autoimmune response. Statins, particularly simvastatin, have been shown to induce apoptosis in many types of cells, including B lymphocytes, cardiac myocytes, hepatocytes, vascular smooth cells, and human skeletal muscle cells [30]. How statins exert this proapoptotic effect is unknown, but the mechanism may involve protein prenylation, an effect reversible by mevalonate [31]
Current users of statins for 10 years or longer had a 1.83-fold increased risk of invasive ductal carcinoma (IDC) [95% confidence interval (CI): 1.14–2.93] and a 1.97-fold increased risk of invasive lobular carcinoma ( ILC) (95% CI: 1.25–3.12) compared with never users of statins. DOI: 10.1158/1055-9965.EPI-13-0414 Published September 2013 Long-Term Statin Use and Risk of Ductal and Lobular Breast Cancer among Women 55 to 74 Years of Age
“Statin-induced lung injury (SILI) is an uncommon but serious pulmonary complication. The clinical features and outcome of patients with SILI vary widely.”
“Statin therapy may be associated with a variety of musculoskeletal disorders, including myopathy, myalgias, muscle weakness, back conditions, injuries, and arthropathies.3 These disorders may be particularly problematic in older people and may contribute to physical deconditioning and frailty. Statins have also been associated with cognitive dysfunction, which may further contribute to reduced functional status, risk of falls, and disability. The combination of these multiple risks and the ALLHAT-LLT data showing that statin therapy in older adults may be associated with an increased mortality rate2 should be considered before prescribing or continuing statins for patients in this age category.”
“Fifty consecutive new cardiology clinic patients who were on statin drug therapy (for an average of 28 months) on their initial visit were evaluated for possible adverse statin effects (myalgia, fatigue, dyspnea, memory loss, and peripheral neuropathy). All patients discontinued statin therapy due to side effects and began supplemental CoQ(10) at an average of 240 mg/day upon initial visit. Patients have been followed for an average of 22 months with 84% of the patients followed now for more than 12 months. The prevalence of patient symptoms on initial visit and on most recent follow-up demonstrated a decrease in fatigue from 84% to 16%, myalgia from 64% to 6%, dyspnea from 58% to 12%, memory loss from 8% to 4% and peripheral neuropathy from 10% to 2%. There were two deaths from lung cancer and one death from aortic stenosis with no strokes or myocardial infarctions. Measurements of heart function either improved or remained stable in the majority of patients. We conclude that statin-related side effects, including statin cardiomyopathy, are far more common than previously published and are reversible with the combination of statin discontinuation and supplemental CoQ(10). We saw no adverse consequences from statin discontinuation.”

Thanks for that – the very title of that article shows the visceral nature of this debate. The angry people know they are on shaky ground, and need to resort to such language to try to stop people learning the truth. The awful part is that this isn’t the only group of researchers who are called denialists – those who ‘deny’ that HIV is caused by AIDS get the same treatment. To me that means the establishment is probably also trying to fight an awful truth. Here is what a Nobel prizewinner in biochemistry had to say on this subject:http://www.duesberg.com/viewpoints/kintro.html

The true scale of the scandal of corrupt science may be almost unbearable.

Gary, I was tempted to mention Climate alarmism, but I thought another possible/probably medical story was more relevant. The terrifying thing is that the anti-AIDS drugs are given to people with no symptoms (and even now are offered to HIV negative sexually active homosexual men), and over time some start to show symptoms, but there are suggestions that the symptoms are also those associated with the side effects of the drugs themselves! On top of that, the HIV test is more likely to come back positive if the patient has received certain vaccinations recently, or is pregnant, etc.

David Bailey: Yes, HIV/AIDS is mostly scam. Virology is actually pretty bizarre. Viral particles are usually detected by indirect means. They’re so small that to be detected there must be10 to the 23rd particles. That’s a really, really, really big number. There was a film, banned in London, but available on line. I forget the name. It concerned five people in Spain who were HIV positive for nearly two decades, but all had refused the extremely toxic (chemotherapy agents which had never been licensed for this reason) “anti-retroviral” drugs, and none of whom ever got “AIDS.”

I’m someone that thinks statins do a bit of good – tiny bit – NNT 83 at 5 years – nothing to brag about. Yet – with they start using ad hominem attacks, you know they have lost the debate. The tide IS turning.

My guess is lowering LDL is a side effect of statins. ( There is a long list of LDL lowering drugs that don’t lower mortality).

I figure that statins don’t prevent CAD – only limit the result of the damage – slightly – possibly by changing unstable plaques into stable calcified plaques – or a slight increase in NO.

The cause isn’t just mechanical – but I’ve wondered if once there is a blemish on the smooth lining if there is positive feedback and more happens.

I don’t think LDL is causative – not important if it gets in the front-door or the back-door – what matters is what causes the first blemish – which I think is likely a thickening in the way inner intima – that limits circulation.

If it was just mechanical – I would expect a better correlation with blood pressure – or any athletic activity.

My hunch is still insulin/cortisol – perhaps something that reduces the NO response?

I don’t understand why tadalafil wasn’t further studied for CAD? Was there unpublished research? My gut tells me it might be a better treatment.

Xtronics,
1Statins are ‘prescribed’ by doctors and recommended by national medical authorities.
2: Often the doctors are using the ‘threat’ of death to enforce compliance by patients
3: Many national governments are subsidising the cost of these prescribed drugs. so there is a huge public finance burden.
4 : There are now known serious side effects on people who take statins
5 : They are prescribed in order to lower LDL-C not with any other ‘goal’ in mind.
6 : There is a very limited improvement in the health status of people taking them.
7 : Because this statinist ideology holds sway, research into more effective ways of preventing or curing heart disease does not get funded or get priority.

Looking at this big picture that is a complete fuck up.

Remember medicine’s first principle ? “First do no harm “. It has got lost.

Hey xtronics – I always looked to you for the science at TYP (hope all is well there. As far as statins are concerned, Google Stephanie Seneff and Cholesterol Sulfate. It’s a theory that make more sense than anything I’ve heard in years. If you buy any part of it you may rethink the statins value.

“I’m someone that thinks statins do a bit of good – tiny bit – NNT 83 at 5 years – nothing to brag about. ”

I suspect most people would turn down statins if their NNT of 83 over 5 years was explained to them. When I started taking statins, I assumed that the gain from taking them was far, far greater than that, and I am sure others do too. I have come to realise that everyone should be told the NNT of the drugs they take. I know one guy who struggled through several changes of statin type, and each time he suffered both memory loss and muscle cramps. If he had known the NNT value, I am sure he would have stopped much sooner. Indeed, I think doctors would become embarrassed by large NNT values, and stop prescribing some of these drugs!

I would say that if I hadn’t realised my cramps were caused by the statins four years ago, I would be far less fit by now, because I simply couldn’t have gone out walking or cycling. There are also people who report permanent statin muscle problems!

David,
I think NNT is a difficult concept to grasp. You could look at it like this:

“After taking a statin a day for five years, i.e. 1,825 pills, you will have a one in 83 chance that you will have avoided a heart attack. In other words, there is a 98.8% chance that they will have done you no good whatsoever, and very likely some harm.”

The main reason for my belief is that I don’t think I would have been alive today if I had embraced any of their medical suggestions all those years ago.

And of course this blogs adds to my “disbelief” on this matter. E.g., cardiologists in general actually “hate” us “statin-deniers” and I guess that hate is the only thing they can come up with since cardiology science strongly seems to be on our side of the fence.

I want to revisit fluid dynamics, along with your statement: “In general, if you look at where atherosclerotic plaques develop, you find that they most often occur at maximum biomechanical stress.”

I’m developing a Vortex powered kinetic marine energy extraction device and I’ve come to admire Vortex formation. They are a key component of fluid dynamics and my research has shown that with the correct conditions they will form EVERY TIME. (Think of an airplane wing creating lift every time it reaches a specific starting speed)

Vortexes will accelerate the fluid and create a pocket of differential pressure. If you are one of the people unlucky enough to have the correct conditions for formation of Vortexes you could expect a little over one Billion beats between years 20 ( when the heart finishes growing ) and year 50. That’s one billion vortexes forming on the same spot, over and over again.

It’s not just the pressure within the arteries but possibly the specific shape of the artery. This could explain family clustering of CVD, DNA creating similar conditions for vortex formation within family lineages.

This could be a mechanism outside of just straight pressure that causes long-term repeated stress at one specific spot which finally translates into damage that needs repair. That damage could happen just downstream of the vortex formation site, allowing repeated damage to happen. The Vortex forms just slightly downstream of the formation mechanism.

As an aside, anyone try taking honey before bed yet? Three months of amazing sleep has me a believer. After all we do spend 1/3 of our life in bed. I’ve found honey has stopped all my night time stress ( i.e. bad dreams, I still have the same dream but amazingly there is no stress associated to it and therefore I don’t wake up. It’s all quite remarkable. ) Go ahead and try it, two tablespoons of honey (don’t skimp) once in your life before bed isn’t going to kill you. We’re all use to n=1 experiments. Try it (peer pressure) you won’t be disappointment.

Shameless Plug – If anyone is interested in seeing my device you can google ( and youtube) Vortex Power Drive (.com) and if anyone is interested I am looking for an Angel (wink wing, nudge nudge)

Doug, I have not a cent to offer as an angel for your work. Sorry !
But I think your comment about vortexes in blood flow being increased at arterial ‘junctions’ is important. Yet another piece is the complicated jig saw puzzle towards the big picture of what causes heart disease. It fits with Martins comment about the endothelium cells in the artery being aligned with blood flow. And that at arterial junctions, this streamling is necessarily distorted. Thank you

Similar article in the Daily Mail today. Apparently ‘the benefits of statins are so clear they should be offered to patients in their 30s and 40s’ .. who are largely healthy but .’who have high cholesterol’. This is the good thing though – although the study was part funded by drugs firms who make statins the researchers said ‘the manufacturers had no influence on either the design of the trial or the results’. What a relief, we can relax and believe everything they tell us now.

The DM seems to print health and other science articles without any editorial input or cross referencing at all! I suspect other papers are similar, except that papers such as the Guardian censor articles that cast doubt on Climate Change (and possibly on other subjects?)

Thus in the DM you can read pro and anti statin arguments, arguments in favour of fat and salt reduction, and articles pointing out the research that show that this has no benefit, hand wringing articles claiming that climate change is causing hurricanes, and other articles pointing out that there have always been hurricanes in certain parts of the world, but that the growth of population that makes these ever more dangerous.

Yes. It is an interesting question. It is, in my opinion, for two reasons. One blood pressure/flow/turbulence/shear stress is much lower, thus there is no endothelial stress/damage. Secondly, because tissue factor is not present in arterioles, to the external trigger for blood clotting does not exist.

Odd how we make these single character typos that we miss because the word is not a misspelling.
Above I wrote “hepatic portal of the lymphatic system” meant to be “hepatic portal or the lymphatic system”.
I assume you meant, “so the external trigger for blood clotting does not exist”.
Probably, like me, as soon as you posted you saw the mistake. Something changes in the visual field, or maybe there is a change in the feeling of stress – after posting you relax.
In some ways, this is what you are doing with CVD. The researchers are not standing back from what they have ‘written’ they are too busy ‘writing’ the next bit. Somehow, we have to change context to see the errors.
That tissue factor is not present in arterioles also has a wider message, we do ‘work’ we don’t need fixing most of the time, ‘nature’ seems to have everything under control.

It’s interesting that in all the thousands of millennia it took for mammals – and us – to evolve, there was never a successful mutation that avoided pressure, turbulence, and shear stress damage, obviating the need for damage repair. Gotta have those bifurcations.
Evolution was efficient enough, though, to avoid unnecessary Tissue Factor where damage was not happening.

There’s really no damage? Even with those little vessels getting squashed with each beat?

JD, I have been thinking about your question of why exercise is beneficial to the heart when it imposes extra stress.

It seems true as a general priciple, that he have all inherited from evolution, a command instruction that says ” Use it or lose it”

In an evolutionary context, what is not used is interpreted at a cellular level as not needed.

This is obvious in cave dwelling species that lose eyesight. But I suggest it is also at work in humans. Our muscles increase in capacity when used. And decline when not used. Exercise thus simply using muscles. And the heart is a muscular pump.

However I have no idea how this takes place at a cellular level. There, I have no idea !

Bill in Oz: The paper that JDPatten linked to explains, at least partially, what happens at the cellular level due to exercise. What I know for certain is that it sure makes me feel good! Today (Sunday) is a workout day, and that makes me happy.

Bill and Gary,
First, there’s your “original equipment” that your genes provided you. Then, there’s how it responds to what you do with it. Some of us thrive on hard exercise, and some of us not so much.
I enjoyed weight training as a teenager. I enjoyed moving heavy logs and stone slabs around as a sculptor. Same, working as a stone/brick mason, cutting and splitting firewood.
I felt good being strong and capable.

In my late fifties and early sixties I got atrial fibrillation as my CAC was piling way up.

I strongly suspect that too much was too much – – – for me.
Even though it felt good. It felt right.
Fool me.

JDP, I still love doing some dry stone rock walling. And a session at the gym leaves me happy and feeling all’s right with the world… Such is ‘exercise’.. But my younger brother is past such physical,work now..Yes it all depends on the individual person..

Off topic here but related in a way. I haven’t been receiving email notifications of new comments for the past two posts. This morning I did get one – from the ‘Turning Diabetes on its head’ post in 2015! What’s occurring? Ticking g the boxes dutifully again. Ooh I’ve just noticed that my email address is wrong by a letter. Goodness knows why or how but I’ll just change it and see what happens.

I think I may have cracked it as I just had one of the ‘confirm following’ emails. I honestly never touched my email from the time I joined this blog. So if it happens to anyone else, check your email address in the box. For some unknown reason the ‘n’ in my name had changed to an ‘m’. It must have been Harvey as my mother would have said!

Recently came across this report via UNICEF regarding the Polio Vaccine being used in war torn Syria:

In war-torn Syria, there’s little doubt that the conflict has taken a toll on health. Now, the United Nations Children’s Fund (UNICEF) reports that their attempt at using vaccines to “protect” children against polio has backfire — infecting more children with the devastating disease rather than saving them.

Vaccines make children sick, you don’t say?

As World Health Organization representative Elizabeth Hoff reports, “As of 18 August 2017, 33 children under the age of five have been paralyzed. The detection of the circulating vaccine derived polio virus type 2 (cVDPV2) cases demonstrates that disease surveillance systems are functional in Syria. Our priority now is to achieve the highest possible polio immunization coverage to stop the circulation of virus.”

Thirty-three children paralyzed by the vaccine that was supposed to protect them — and the UN’s response is to just keep doling out more vaccines? Sadly, that’s par for the course. Obviously, bad medicine is never the problem — there’s just not enough bad medicine, that’s all.

Mark Johnson: Her words are astonishing: “We’re paralyzing them, and to stop paralyzing them we’re going to keep paralyzing them.” This is precisely why the OPV was de-licensed in the U.S. in the year 2000! Have these people lost the functional use of their brains?

If she were to say otherwise, she would end her career. Most scientists refuse to question vaccines and their effectiveness, they take it for granted. meanwhile…children are dying and vaccines are shedding, they shed unto vaccinated and unvaccinated alike. Vaccines and vaccination is a religion now. Those who dare question it are deemed as profaners.

My theory is human beings have evolved with viruses, microbes, bacteria and so on for ten of thousands of years, they are part of who we are, we grossly have 10 pounds of them into our guts and skin. they live in harmony with us, most of the times anyways. injecting dead or alive viruses along with adjuvents into our blood stream (aluminium or what not) is complete non-sense. that is not how our immune system works. the only thing vaccines do, is create turmoil and the human body does its best to take this crap out of the blood stream. there is no long life immunity from vaccines whatsoever, at best they prevent the onset of symptoms for short period of times. This is another scam perpetrated by pharmaceutical companies and their salesmen.

“Recently, researchers in Lyon, France, prospectively studied the effects of the Cretan Mediterranean diet on a group of 605 postmyocardial infarction patients (9). Patients were randomized either to the Cretan diet or to a “prudent” diet similar in composition to the American Heart Association Step 1 diet (control group). All other aspects of the patients’ health care were identical. An astonishing 70% reduction in the incidence of subsequent death and nonfatal myocardial infarction was reported in patients on the Mediterranean diet after a mean follow-up of 27 months, a ratio that was maintained through a final 48-month mean follow-up (10). Even more remarkable is that this mortality benefit occurred despite no difference between the study and the control populations in follow-up LDL and HDL cholesterol levels and only a very modest 6% drop in total cholesterol levels in both groups from 250 mg/dL to 237 mg/dL. The magnitude of benefit reported with the diet alone should be contrasted with that achievable by other routine secondary prevention therapies, including statin drugs (35% event reduction) (11), beta-blockers (15% reduction), and angiotensin-converting enzyme inhibitors (20% reduction) (12).”

This study dates from 2000. But it is still very interesting. I looked through the various sources used by the authors for this paper. Note 10 lists this source ” Mediteranean Diet, Traditional Risk Factors, and the Rate of Cardiovascular Complications After Myocardial Infarction : Final Report of the Lyon Study” by Lorgeil, Salen, Martin et al,
This is actually more interesting and valuable than the the ncbi one linked above.

The Lyon study compared the outcomes of 2 groups of heart attack patients who were assigned randomly to one of 2 groups. However the diet of the control group was not investigated at all. These French individuals received no advice of a dietary nature during the trial.

The experimental group however were individually advised and coached into adopting a Mediterranean diet. And there was a degree of close observation to ensure compliance.

Also “none of the patients were not fully informed that they were participating in a dietary trial with the comparison of 2 diets.” page 784

The results of this process were quite good.
“The rate of cardiac death and nonfatal infarction in the experimental group after 46 months (1.24 per hundred patients per year) is similar to that observed after 27 months (1.32). ……..
The rate in control subjects was 4.07 after 46 months, whereas it was 5.55 after 27 months. Hence, the data confirm the impressive protective effect of the Mediterranean diet.”

Effectively there were 4.3 fewer deaths per hundred patients in the Medierranean group.

Also a little speculation is warranted: This was a research trial done in Southern France in Lyon with French patients. I wonder how many of the control group patients were also, of their own accord, due to their own dietary preferences & culture, eating a Mediterranean diet ?

Remember the diet of the control group was not assessed or discussed with them

Is there really a definition of a “Mediterranean diet”? I suspect it’s a bit like the perception of a “healthy diet”, and could mean almost what you want it to mean. Judging by the size of many of the older people in such places as Italy and Greece, it doesn’t seem too good a diet.

I guess we could go look in the reports of the Lyon Diet Heart study and see what the trial researchers meant in th3e 1990’s by “Mediterannean diet”. But I gather it included lots of vegetables, legumes & beans, fruits, olive oil, occasional dairy, regular but limited red wine, some fish & very occasional meat….

As for people there being obese, I cannot comment having not been there to Greece. But it could be a recent phenomenon from the prosperity of the 1980’s – 2008.

AH Notepad: Correct. There is no such thing as the “Mediterranean diet,” but a multitude of various diets in this vast region. The “Mediterranean Diet” was invented by nutritionists. Chapter 7 of “The Big Fat Surprise” explains this in great detail.

“Patients allocated to the Mediterranean diet (n = 302) received a 1-hour educational session outlining the diet (more bread, root and green vegetables, fish, poultry, and fruit; less meat; and butter and cream replaced with a rapeseed [canola] oil-based margarine provided by the study, or olive oil). At 8 weeks and then annually, a diet survey and further counseling were completed. Control patients (n = 303) received standard dietary advice from hospital dieticians or attending physicians. “

During the 1 to 5 years of follow-up, patients on the Mediterranean diet consumed more bread, fruit, and margarine, and less butter, cream, and meats than patients in the usual diet group (P < 0.01). Patients in the Mediterranean diet group had fewer deaths from cardiovascular causes (3 [1%] vs, 16 [5.3%]…"

The conclusion seems to be that it is the higher proportion of α-linolenic acid i.e. omega-3 fatty acid, that makes the difference.

Martin I too am perplexed by this ‘Mediterranean diet’ used by the Lyon researchers, with the reduction in dairy and the increase in margarine. That is so 1970’s-80’s. And since then we know from lots of studies that saturated fats are not a cause of heart disease.

My guess is that the study dates from the time when this was the ruling ideology. When lots of us were all scared off butter and normal fat milk and ate margarine instead. Vuriously in my 6 months in France in the late 1970’s hardly any French people that I knew ate margarine. Butter & saturated fats were the norm. And that was the time of the French paradox !

I wonder if anyone has thought of repeating the trial with an improved diet for the trial group. .

Well those results don’t fit in with my beliefs, so I will take the unscientific approach and not believe the results. I’ll carry on avoiding carb, and eating the cream, butter, eggs, veges, fruit etc.
Canola and soy oil don’t strike me as safe. If you can put it in a truck and start the engine, it ain’t food.

I did a google search about Mediterranean diet.. And up popped a page on the ABC’s Catalyst web site from 2008 with a certain Scottish doctor ( initials N S )..He did a video & interview of a Greek expert on all the benefits of a Cretan Mediterranean diet.. No margarine at all mentioned.

I am ‘conflicted’ whether to give him the time of day and look at it.in the interests of gaining knowledge. Or just move on to something else as he was an arrogant bastard even in 2008.

One can be arrogant, and still be right. I try to put aside my opinion of the person holding views – but it is difficult. There is a certain Prof Sir R C who stirs certain emotions in my breast that make it tricky to read anything he writes, or listen to anything he says, with the required dispassionate scientific equanimity.

Thank you Dr K. Yes, it’s a difficult thing to do but worth it.
Moving on from NS, this past hour I have been watching a new Catalyst program about heart surgery hosted by Perth based heart surgeon Nicki Stamp. She interviews 6 heart patients that she has been involved in helping.One is a 2 year old little girl named Sophia. Another is a 94 year old active woman named Betty. And the others are male & female of all ages in between.
It is a really informative & heart warming progarm. The best I have seen from Catalyst in a long time.

Yes Martin I suspect that even better results could have been achieved if the Lyon trial had actually based the experimental diet on real science instead of nutritional ‘hunches’ about Cholesterol & saturated fats…

Bill in Oz
You are being slightly hard on de Lorgeril, he put the trial together very quickly, against opposition, and it was all written up in 1999. France tends to be fairly conservative, and especially the medical profession. We have moved on since then, but his conclusions rest largely valid. I think Dr K ‘s book, the Great Cholesterol Con, only dates from 2008?

Mr Chris, Yes this study was done in the 1990’s. So it is a bit outdated in the light of more recent research since then about LDL-C and saturated fats.

But I had the odd experience of having the Lyon Heart diet trial cited at me a few months. ago by a major nutritionist ( Rosemary Stanton ) here in Oz. In her eyes it was still valid and she is in 2017 recommending that diet here. – but maybe without the margarine. I am Not sure about that aspect of her thinking.

Bill
The margerine has always struck me as odd, but the interesting thing is what can be done with tweaking diet.
As regards the Mediterranean diet in general, and the Cretan version in particular, it is interesting how there is so little consensus. I havé Heard it said that the Cretan diet should be that of the mountains, since only there van be found the propre spelt flour!

A number of accounts that I have come across feel that the main difference in the outcomes lies in the difference between the control diet and the experimental diet omega6 : omega3 ratios.
(for one, Dr Michael Greger – a vegan who professed dismay at the Studies results)

I am not really interested in a vegan’s opinion.. But I wonder where he expressed his dismay.. I have not seen it referred to before..I guess it simply means he’s got it wrong..

By the way Denise Minger did a review of his new book back in May on her blog. A lengthy detailed review of Gregers inaccuracies etc

And yes it may be that the real reason for the difference between the control & the trial results for the Lyon Diet study may be the different levels of consumption of Omega 3 & Omega 6 oils.

But remember this was France & French people. And the study did NOT examine at all what the control group were eating…

So we know that the trial group people after 4 years had a lower mortality rate ( 3.5% )..because they were eating the recommended ‘Mediterranean’ diet.

But we have no idea what members of the control group were eating or if some or them ( and as this was Southern France, maybe a lot of them ) were also on some type of Mediterranean diet…And this would have decreased mortalities to some extent

Meanwhile the trial group were eating industrial oil margarine.. Which I suspect would have increased the number of mortalities in this group to some extent..

There is no such thing as a Mediterranean diet. There is probably even such a thing as THE Mediterranean diet. It was made up by Ancel Keys. France, for example – lowest CHD rate in Europe or, indeed, the Mediterranean – has a bit of coast on the Mediterranean, more coast on the Atlantic, and the diet bears bugger all relationship to what they eat in Crete. Maybe a bit of olive oil (more saturated fat per gram than a steak). Whenever I see anything written about the Mediterranean diet (and I have visited, and eaten, in every country with a coastline on the Mediterranean, other than Libya and Albania) I mentally do my crumble, throw, bin, exercise.

DR K, I have to admit I am biased. When I think about ‘Mediteranean’ diet, I automatically think of ‘peasant’ Greek food, courtesy of growing up in Melbourne in the 1960’s & 1970’s when it was the city with the second largest Greek population in the world- right after Athens !

Later Lebanese refugees arrived and brought with them a different version of the ‘Mediterranean’ diet with homus, tahini, falfels etc. But with many dishes very similar to the Greek ones already adopted…

As for the French, yes there things get complicated. I well remember eating at restaurant in Rue de Navarin in Paris. It had cheap food but the staple was “Bif teck et des frits’. Steak & chips in the UK !
And then French ‘Haute Cuisine’ is very very different again. Both to to Greek food & English food. However it is the food of the aristocrats, the wealthy and their admirers/copiers with no resemblance to Mediterranean cuisine. But the older southern french peasant cuisine has some similarities with olives and olive oil & red wine, vegetables & meats..
And after all this pondering, I wonder what the Lyon Researchers recommended to their trial group of patients in the 1990’s – apart from margarine ?

Bill in Oz: I fully agree. Dietary studies have so many confounders, and the data themselves have questionable reliability, and thus value. I am participating in a dietary study, just for the halibut. Answered the first (demographic) questionnaire yesterday.

.
Bill, If you are feeling strong you can listen to Greger expressing his views in a video “40 Year Vegan Dies of a Heart Attack! Why? The Omega-3 and B12 Myth with Dr. Michael Greger” 2003https://www.youtube.com/watch?v=q7KeRwdIH04 . . . It only lasts 1:16:33

On the Mediterranean diet (and the so-called French Paradox) . . . After 3 years of LCHF and reversing T2D a couple of months ago I was on holiday in France and spent 3 days staying with French friends. Eating wise I had to just go with the flow . . . Bread with each meal, sweet biscuits specially cooked by the man of the house, sweet apple tarts, potatoes, pasta . . . cannot say we were overwhelmed with vegetables and fruit, but did have good meat. . . And breakfast (more bread/toast with the coffee) – I do not have breakfast as a rule, but you have to be polite. My wife put up a picture of me enjoying a wonderful ‘extra’ biscuit on Facebook captionning “I am the one who will have to listen to him complaining about putting on weight and his sugar levels”.

The aftermath: At the end of the 3 days . . . weight at the end was unchanged from the start. Couple of days later at home testing fasting glucose . . . still the usual 5.1 mmol/mol. I came out unscathed. (Perhaps for real ‘scathing’ I needed more than 3 days).

The diet during the visit was typically French, the same one that I had enjoyed with these friends and other French friends on and off over the last 50 years. Not in a million years would I have called it Mediterranean . . . But then a spooky thought! (Hit the Twilight Zone intro) . . . perhaps during my stay, my apparent resistance to the high carb diet was because I fell under the influence of . . . . The French Paradox!
😉

PS Anthony, re Dr. Greger : I looked the Youtube link you posted from 2003…
I did not really want to waste 1 hour 16 minutes of my life watching him..His opening statement about the founder of Wendy’s put me off..His logic went like this
1: The Wendy’s hamburger founder died of a heart attack
2: He ate hamburgers
3 : Hamburgers cause heart attacks
4 Meat eating kills
Duhhhh ?
Excuse me but what about the sugared up buns ? What about the industrial oils the burger patties are cooked in ? What about the fries sold with the burgers ? What about the reused industrial oil the fries are deep fried in ? What about the Coke & Pepsi sold with the burgers ?
What about the non meat ingredients used in the processed burger patties ? What about the tomato sauce ( ketchup ) loaded with sugar sold with the burgers ? What about the mayo loaded with sugar & industrial oil, also sold with the burgers.

Do none of these industrial processed food items have any role in causing il health and death ?

I then went & looked at one he gave in 2016 promoting his book “How Not to Die” Why ? Just to take a look at Greger more recently..And that turned up something interesting..Still slim. But he has definitely aged a lot.. Far more than I expected for 13 years…In the 2003 Youtube he looks in his mid thirties. In the 2016 Youtube he looks in his late 50’s. Plus long flowing hair to almost no hair in 13 years.
Now I wonder which of the foods in his vegan diet have caused that fast aging to happen.

I watched his 2016 talk. But after a minute or so I’d had enough. Listening to his nasal quick fire prepared speech put me off entirely. A New York Yankee Jew is full overwhelming bomb mode !

That’s an extreme position. It’s a bit like trying to define the colour blue. To me it’s a royal blue; others might nominate a sky blue or turquoise or aquamarine or powder blue or cyan or… The term “blue” is a flagpost rather than a fence, suggestive rather than definitive, until defined by a committee and ratified by common usage.

It seems to me diets can be broadly classified by ecological region. My imagined diet would be a mountain diet. You could also get a coastal diet (fish and shellfish based) and a plains diet (large herbivore based) in temperate regions. In polar areas you’d get a tundra version of coastal or plains diet; in the tropics you’d get a jungle diet (small animals and fruit) as well. Presumably in the Amazon there is such a thing as a riverine diet (fish and crabs), but maybe it’s just a freshwater version of a coastal diet. All diets would be modified by exchange with neighbouring regions, but the broad outlines should be as recognizable as the colour blue.

If everyone can imagine their own Mediterranean diet, then there is no such thing as a Mediterranean diet. It is either a clearly defined diet, or it is not. I have never seen it defined – in any real way. I have seen that it may consist of certain items, olive oil, fish (there are hardly any fish left in the Mediterranean, most of it is shipped down from the Atlantic via Scotland), fruit, vegetables…. healthy stuff. Healthy, healthy…stuff. Pizza, no. Pasta, yes, but not too much, fruit – what fruit. Avocados? No, bananas – probably not. Just the healthy type fruit, type of fruit stuff – you know. Lots of different colours, all right, stop being to picky. Vegetables yes. Potatoes…no. Chips, terrible. They are clearly not vegetables. You may sense my frustration with the indefinable Mediterranean diet. It is, whatever you want it to be. And good luck with that.

Larger surgeries trigger an inflammatory response which are described under the term “surgical stress” and may result in increased cardiovascular complications. The underlying mechanism seems to be endothelial damage. There is some evidence that high doses of methylprednisolone reduce circulating markers for endothelial damage such as Syndecan-1. Glucocorticoids prevent inflammatory shedding of the endothelial glycocalyx and may stabilize the endothelial barrier function ( Lindberg-Larsen V, Ostrowski SR, Lindberg-Larsen M, Rovsing ML, Johansson PI, Kehlet H, The effect of pre-operative methylprednisolone on early endothelial damage after total knee arthroplasty: a randomised, double-blind, placebo-controlled trial. Anaesthesia. 2017 Jul 26; and Chappell D, Hofmann-Kiefer K, Jacob M, et al. TNF-alpha induced shedding of the endothelial glycocalyx is prevented by hydrocortisone and antithrombin. Basic Research in Cardi- ology 2009; 104: 78–89).

So it looks to me that the glycocalyx is the first layer of protection that gets destroyed before the endothelial cells are hit.

That would make sense. Of course, one could turn it round and say that, damage to endothelial cells damages their ability to create the glycolax. In reality, it doesn’t matter the direction of part of the causal chain. Damaging the glycolox exposes endothelial cells to ‘toxic’ substances/forces that can create enough ‘stress’ to strip them off.

And now for someone else’s take n the causes of heart disease. I do not have the medical training to assess this article by Dr Tom Cowan.
But it seems to be a good one. It discusses the role of stress ( caused by a multitude of things, physical , emotional etc ) and the adrenal gland response.https://www.westonaprice.org/health-topics/adrenal-heart-connection/

An additional comment : when I posted the note above I had not got to the sections where Cowan discusses Rudolf Steiner’s thoughts. I am skeptical bout this part and thin kit unnecessary and does not add much to the substance of his argument…

Bill in Oz: Rudolph Steiner had some interesting insights into the influence of the heavenly bodies on the growth of plants, but I am skeptical of what I’ve read of Dr. Cowan’s ideas concerning heart disease.

Gary, I am a firm adherent to the ‘Ockham’s razor’ principle. When attempting to explain something, keep it as simple as possible withing the known facts.
Cowan could have written that article without any reference to Rudolf Steiner. But he threw it in anyway.
Why I wonder ? To signal to readers his own personal philosophical beliefs ?. Or Virtue signalling ?
That makes me uneasy. However the rest of it had much information ( facts ) which is useful. His 10 years as a doctor in a US hospital ER provides a perspective which is worth thinking about.
So I am interested in knowing why you are skeptical.

BTW : I know of Steiner & have attempted to read his writings. For many German speaking peoples, he is a genuine philosophical genius and hero. But for most his is a fringe religious figure. So here I will not go there.

Bill in Oz: I agree about Ockham’s razor. My only knowledge of Steiner is through the principles of biodynamic farming and gardening, which make sense to me, and some of which I utilize (such as planting and harvesting root crops with the waning of the moon, and surface crops with the waxing). I haven’t read Dr. Cowan’s piece that you refer to. My skepticism is mainly due to my skepticism of WAPF, of which he is a board member. They have promoted some things which I think are dangerous, and I cancelled my membership. Stephanie Seneff does publish in their journal, and speaks at their conferences, and I consider her a meticulous, first-rate scientist.

Gary, I suggest you look at the Cowan article. Perhaps not all of this particular article is nonsense. As for the Weston Price Foundation a few years ago Sally Fallon published some very aggressive articles attacking vegetarians. And then published a review attacking one of Michael Pollan’s books. I did not renew my membership after that. But i occasionally brouse the web ste. It does have some well informed writers like Masterjohn and views that we would otherwise be ignorant of.

Bill in Oz: Absolutely right. Much good comes from this organization; many fine speakers at the conferences. The problem is, it is run like a dictatorship, the board merely a rubber stamp. Her attack on Paleo, and two years ago, on those who questioned the safety of the cod liver oil she promotes cost the foundation about a third of its membership. Sad.

I love this part of article since it strongly relates to the state in my own coronary arteries.

“Let’s dissect this scenario a little bit. First of all, when a cardiologist shows a patient a diagram of the heart, it shows the four major coronary arteries going to the heart. All cardiologists show patients the same diagram of the heart with these four blood vessels. They show the stenosis and say, “It’s 97 percent blocked, you’re only getting 3 percent squeezing through the bottleneck.” They just told this person who’s sitting there looking totally fine that he’s got 3 percent blood flow to one of the major parts of his heart. Think about that. How is he even sitting there? If that’s the only way he gets blood to his heart, how did the patient walk up the hill, albeit with some difficulty? Moreover, the cardiologist says that if another 2 percent gets blocked (so that he is down to 1 percent blood flow), he’s a goner. Is there any meaningful difference between 3 percent and 1 percent? How do you explain the fact that this guy is even alive? When you put all those pieces together, you start thinking that there is something about the conventional explanation that does not make any sense.”

Are cardiologist in general stupid or just criminal?

Yesterday we met with a couple of my own age – both on statins. The man was diabetic and was taking insulin. The woman told us she had had a stent inserted.

So we told our own stories of how it to our own experience is possible to avoid heart surgery and medicine and how to revert diabetes by simply skipping all the carbs and there was a lively discussion as always.

If you to start with good physiological “arguing” and lining up “irrefutable” evidences (in a Popperian sense) showing the great flaws in present day cardiology and medicine you don’t have to invoke supernatural (religious) causes as a way out of this in my mind as an old researcher in the natural sciences.

Here is the summary from the article link above:
• Impaired sulfate supply to the heart is a key factor in cardiovascular disease.
• Red blood cells, platelets and cells in the skin synthesize cholesterol sulfate catalyzed by sunlight.
• Cholesterol sulfate, unlike cholesterol, is water soluble, so it can travel freely in the blood rather than packaged up inside an LDL particle.
• Glyphosate, the active ingredient in the pervasive herbicide Roundup, disrupts sulfate synthesis in the skin and disrupts bile flow from the liver, leading to a systemic deficiency in cholesterol sulfate.
• Sulfate provides negative charge in the blood vessel wall and for the red blood cells and platelets, promoting flow.
• Sulfate also maintains the structured water that lines the vessel walls and presents a slick, frictionless surface to the red blood cells.
• The atheroma actively recruits cholesterol to be ready to produce cholesterol sulfate when sulfate becomes available.
• Inflammation, while damaging to surrounding tissues, performs a useful service by promoting an oxidative environment necessary to make sulfate.
• A heart attack is a well-choreographed sequence of events aimed to restore sulfate supplies by oxidizing taurine, which is stored in large amounts in the heart.
• Statin drugs, by reducing the supply of cholesterol sulfate to the heart, will lead to heart failure down the road, a worse prognosis than cardiovascular disease.

Indeed, there are many feedback loops in maintaining homeostasis. If one bit fails first it does not imply that all the other factors in the balancing act were OK.
Why did the Titanic sink – clearly the hole in the side. But, the steel was weak at the water temperature, there were no binoculars in the crows nest, the captain was rushing great circle because of a bunker fire, the sea was calm on a moonless night, the bulk heads were not high enough, there was overconfidence in the vessel capability …

Bill – RoundUp is bad stuff but what I am referring to is Stephanie Seneff’s sulfate theory. She mixes the two in her talks but low sulfate does not require RoundUp but RoundUp may cause low sulfate. Another part of her theory that interests me is that sunshine isn’t just for Vitamin D – it also activates cholesterol sulfate.

FYI – I mix pool salt and water to the highest concentrations and use it as a spray. Amazingly it kills even the hardest to kill blackberry bushes. You can use the straight pool salt on the ground in places where you don’t want anything to grow for a year or more.

Yes you are right. about this. Seneff says that “low sulfate does not require RoundUp but RoundUp may cause low sulfate.”. And I suspect she is right about the role of sunshine in creating cholesterol sulfate as well.

And thanks for the tip about salt as a herbicide. I have had occasions as. an organic farmer when blackberries were a real problem. But a strong salt solution ? Ummm I will remember that one.

Bill in Oz: You don’t even have to use Roundup to get glyphosate into your system. It is so pervasive now as a contaminate in the food supply that most people have detectable amounts showing up in their urine.

Mr. Chris – remember, it’s pool salt and water in high concentrations. So far I have not found anything it won’t take out – but I don’t have any Ivy to test. I heat the water on the stove (not sure that’s required) so it’s easy to mix. Am using a 2 gallon sprayer.

Note: The wild blackberry bushes here (mostly non-fruiting) cannot be easily killed with RoundUp but succumb completely to the salt mixture in about 3 to 5 days.

Fifty pounds of pool salt is four or five dollars at big box stores. So far I have used a few cups so it goes a long way.

Gary,
Thinking, per se, doesn’t necessarily lead you down the right avenue.
Critical thought and judgement are required. An absence of “confirmation bias” and (what-haven’t-I-thought-of) – – – required.

Gary,
(Metaphors! They bite back.)
OK. When we’re thinking about the issues we’re dealing with here, the “avenue” to take is the one that leads toward the understanding of reality and its functioning, blind alleys along the way notwithstanding.

Newton’s struggles with alchemy took him down a blind avenue. Perhaps he didn’t know that. Perhaps it was fulfilling for him to spend his glucose thinking along these lines. Perhaps it was an esthetic endeavor for him. More power to him. However, it got him, and us, closer to reality only insofar as we can discern the misdirection.

For the same reason it is so difficult and so rare to have logically thinking [ ] [ ]s. Fill in the blanks. We live in mental big stories. Just as we don’t notice the blind spot in the eye, the brain fills it in (even glaucoma can be well progessed before a person realises that there’s a visual problem) so with the story. And, we’re busy people, rocking the boat can cause professional problems (see what happened to Tim Noakes & Gary Fettke, and I have seen the same in other areas of science). Let someone else take the flack.

Alas, it might well be that most of the EU population has glyphosate residues. One recent test on MEPS came back 100% positive with residues over the EU allowable amount in water (https://www.ecowatch.com/results-of-glyphosate-pee-test-are-in-and-its-not-good-news-1891129531.html). Even though the EU is basically non GMO, we eat meats raised on GM soy, we use glyphosate on playgrounds and pavements and on some gardens, and worst of all a number of our crops are desiccated with glyphosate just prior to harvesting. It is insidious.

Frederica, I so enjoy your postings….I find you are so down to earth…if that is not a pun.
I have been fortunate to find sources of raw milk lately, and despite the dire warnings in the press and on telly (Monday 11 September), I am more than happy to indulge in it. However, even though the sources I have are unpasteurised and unhomogenised i.e. merely filtered and chilled, the grass which the cows eat is not organic. In fact, I understand that even foods labelled as ‘organic’ are permitted to have some level of artificial additives. We just do not seem to be able to completely avoid such toxins….but at least we can attempt to minimise our exposure to them.
And as for GM foodstuffs for humans and animals….it is a monster which we will no doubt come to experience, having previously been the stuff of science fiction.

Frederica, ROUNDUP will solve world overpopulation problem. There will be plenty of Roundup ready GMO soybeans and corn for everyone.
“It is very likely that the primary target of Roundup, especially its POEA surfactant, is the mitochondria, which play a key role in the development of sperm cells and sperm motility [19]. In addition, male infertility could arise from ROS damages to mitochondrial DNA”.

It is often claimed that “organic” agriculture can not compete with agriculture based on pesticides and GMO crops.

I just came across an amazing video about an American guy who took over a small farm in the middle of cold Sweden, Värmland. Convincingly he, hands on, shows how he in a very short period of time turned this piece of land into a very productive unit and above all into a very profitable farm. He is working with no-nonsense Permaculture.

To me what he presents is very convincing and encouraging with my present dark view on the world.

Seneff in the Western Price article mentions that 3 of the low heart disease regions are volcanic rock based islands and links this to high sulphate. An attractive idea but I believe the longest living and equally low in heart disease are the people of Loma Lindy in downtown California. No volcanic rocks I would imagine. What unifies all these groups of people in the Blue zone regions, its not their Volcanoes. As far as i can see they eat mainly plant based and whole foods with no or occasional grass fed meat. They also have strong social connectivity, anything else ?

The blue zones riddle (how can they be healthy with 85% carb) has been discussed to death. I do think it is a combination of all of the above, and not eating enough fat to really enter the dreaded high trig/high BG/metabolic syndrome cycle. (That does NOT mean if YOU with your broken metabolism subsist on rice and sun it will do you much good.)

So now sulphate is good for you?
I shooed away from getting a bag of magnesium sulphate because (even ignoring the crystal water in it) with every Mg I would have got twice or more the sulphates. Apart from being a laxative unspecified evilness on the kidney function was mentioned. For some reason I never found a good outline of what SO4 actually does in, or to, your body. Similar with the chloride and other anions.

85% of what? I am in Asia all the time, they do not eat HUGE bowels of rice all day long, in fact many esp Hong Kong are BIG meat eaters. We have apt in Hong Kong, there a lot. I think most people in West imagine more rice eating goes on there than actually does! What is making HK kids obese is Western food, processed food, not rice or traditional food. Take an apartment for a month in HK and see how many Obese people you see!

This discussion seems to refer to’ sulphate’ and cholesterol sulphate almost interchangeably. Are you saying that people don’t consume enough sulphate ions – i.e. that sodium sulphate would be a valuable supplement?

Reread the article by Dr. Seneff – the people of Loma Linda incorporate “sunshine” and exercise such as walking. Sunshine activates CHOLESTEROL SULFATE. No volcanoes required! Everyone I know past 80 and healthy has a direct relationship with the “sun” and “motion”.

“in contrast to most people with this condition, only a third have a BMI greater than 23 (which is the Indian cutoff for overweight) and over a third have a BMI lower than 18.5”

What is going on here? They have circulating glucose but their bodies can’t make use of it, even though they clearly need it. Presumably they are not producing enough insulin, or their bodies have become insulin resistant, through some mechanism different to what is happening in the overfed West. My guess would be not enough fat in the diet to mobilize fat-soluble vitamins, but does anyone know the reason? It is not stated in the article.

FTL: Dr. Jason Fung: That’s amazing work, Sarah. With these detailed records, you can see how LCHF and IF help even with a so-called ‘thin’ diabetic. Asians tend to get type 2 diabetes at lower BMI than North Americans, with the average Chinese type 2 diabetic having only a BMI of 23.7 at diagnosis, not unlike Sarah. Even with a waist of 31 inches, you can have type 2 diabetes. The important factor here is the intraorganic deposition of fat (inside the liver and pancreas) rather than the total fat mass.

The case study – https://idmprogram.com/sarah-patient-profile-thin-diabetic/ I found fascinating, but was really intrigued at the end where Sarah describes:
” Since I started ketogenic diet, my blood sugar would surge during exercise by about 80 points. For example I would started at 110 before tennis, after 45 minutes my BG would 195. I tested over and over. I tried to use chocolate or cheese before exercising, none of which was able to lower or keep my blood sugar from surge.

Out of desperation, I took a teaspoon of coconut oil then went on exercising, I found my blood sugar is remarkably stable during and after exercising. Before I found the secret of coconut oil, I could not begin to walk my dogs with blood sugar at 90, because it would surge to near 200, now I can take a teaspoon of coconut oil, then go to do exercising without experience any blood sugar surge”

Any thoughts on this? Where does glucose come from? (gluconeogenesis or glycogen in liver?) Why does coconut help?

Their insulin is running high in the background whilst serum glucose can stay in ‘normal’ range for 20 years! Meanwhile, Insulin and adipose tissue are ravaging body…You can be thin and type 2 diabetic, you can have Visceral tissue around the organs and still look pretty slim.

If this population is like what I have seen, they subsist primarily on white rice and some lentils. They have no money for vegetables or protein. Most of them are very thin, overworked and malnutritioned. They age and die prematurely and suffer from many chronic illnesses: hypertension, DM, CVD, etc.

My guess is their illnesses are due to severe nutrient deficiencies.

I suggest watching Dr Brian Ames talks on Triage Theory and Longevity to understand what’s going on with these people.

I think you are right. Livestock given food which they as species not are adopted to gets sick and need medication. (Today this is sadly the rule in the factory farms.) Probably these fundamentals apply to humans as well. Weston Price dug into this very convincingly.

His extensive research around the world was summarized in his great book

If you read that book, with your declared interest, you will not regret the time spent.

Honk Kong: They walk everywhere, butchers and fish mongers all over HK, Peanut oil main oil, Veg oils market moved in now , cook with a lot of LARD, eat a lot of PORK, Super family and community focused, they work super hard, I love them and they do not over indulge in rice at all! WE do not even have rice in out apartment as meat is main staple… they also have the longest lifespan in the world now ( that is bound to change re pollution. ) They also have low rates of melanoma ( low omega 6 exposure in traditional diet?)

In 1991 we landed at Kai Tak airport for a 4-day stopover in Hong Kong. As I exited the plane a characteristic smell hit me, and I thought to myself that the whole city smelled like a Chinese restaurant. It must have been the smell of peanut oil.

Slightly off topic, apologies but connected to the Lyon heart study and Blue Zones. What do you think would happen to the burden on the NHS here in the UK if everybody went whole food plant based (throw in fish for those who need some flesh). Yes it is hypothetical in the sense that 100% adherence is fantasy but it is my belief that the economic burden on the NHS would be slashed. Yes there would be job losses, Cardiologists and Oncologist would be made redundant in large numbers. Glaxo Smith Klines share price would plummet but hey ho

Why is stress such a dirty word that people try to avoid?
We shan’t get anywhere until we accept that stress is normal and are willing to talk about it.
It is normal, but the way we express it/react to it can cause problems (and we all express it in one way or another).
Please, Dr Kendrick, don’t do any back-pedalling on your opinion that stress underlies a great deal of heart disease. Beware of giving excess importance to factors which, whilst deserving to be recognised as playing a role, may weaken acknowledgement that stress is of utmost importance.
It may seem old-fashioned for people to hark back to stress as a major factor in heart disease, but that doesn’t make it wrong.

oh but i am sure (that he thinks) bad stress is behind most diseases. The complications arise in defining what exactly happens to the human body after prolonged period of bad stress, anxiety, emotional trauma and so on. Another problem, and a crucial one, is not everybody perceive a situation the same way, thus, there is no one size fits all, which scientists hate. they cannot patent a pill to relieve perception from human beings without causing major side effects. where some people see opportunities, others see misery and so on.

Another thing is, why would distress or bad stress affect the heart particularly, or the kidneys or the lungs, you get the idea. we don’t know what kind of stress is relevant to the heart or another anatomy part. Does it affect the weakest link first?

We don’t, as a rule, jump off cliffs. We may not be aware of or understand exactly what happens to the body when we jump off a cliff but we know it would be an unhealthy thing to do.
Similarly, it would be interesting to know exactly how arteries become stressed by stress – and let’s face it – we already do know a lot about it (and thank you Dr K), but the evidence shows that it happens.
People can easily be waylaid into thinking that taking some supplement or simple action is vital to their cure. So much simpler than thinking about reducing stress effects. Indeed, in some cases a simple action may be all that’s required, but for the rest…?

TS: I must say, although I think it very important to take into the body all the necessary vitamins and so forth, the one thing that makes me feel the best: My weekly hike of 6-8 miles on moderately steep mountain trails, and the lovely people I meet along the way. I think this is key to Pioppi, and all the other places with above-average longevity: plenty of physical activity, especially among fellow humans and other creatures.

If blood pressure, flow velocity, and other mechanical stresses caused injury to arterial walls, wouldn’t people who were physically active be more prone to develop lesions than sedentary people would?

I just don’t buy it. As for simple solutions, why did you reject oxygenation? Oxygen is very active. Isn’t it more likely that all of us, regardless how active or how high our blood pressure is, are continually damaging artery walls? Maybe some people are just better at doing the repairs. Maybe they drink more orange juice steadily throughout the day.

Too little blood flow is damaging, which is why bedridden patients develop sores. If too much blood flow is also damaging, this means blood flow is a J-curve with some sort of optimum. I suspect that optimum has quite a wide range, with a peak somewhere around the 10,000 steps a day level we are currently advised to take.

In the “good old days” (about fifty years ago) newly hospitalized MI patients were forced to be still in the beds for weeks. Half of them died.

Then the head at one ward unit challenged these “rules” and had his patients get out of the beds and be allowed to move around and relax in armchairs for instance. The medical staff at the unit first considered him to be a cool blooded murderer until they realized that the death rates actually dropped from 50 to 20 % and he became a hero instead.

My own idea is to work in my garden as hard as possible in intervals. I am constantly measuring my puls rate to see how high I can get at the age of 71. I am though a little sad to note that this year iI am not able to get above 150 bpm while I was able to reach 160 a couple of years ago.

Göran
Interesting about your pulse, I am 77 and my highest on my bike this year has been 154. People tell me this is dangerous or impossible and my theoretical maximum is something like 130. I point out that if that were the case I would have to live in Holland where you cycle on the flat.
That being so, I do slow down a bit when it gets to those levels

I’m 75 and can get my heart rate up to 190 with really fast walking, though it drops quickly when I slow down, I asked my GP about it as I did feel a tad anxious about it and after the usual questions and appropriate answers he said “Nah, you’re just super fit. Carry on” so I did and do.

Jan B
Well done for your heart rate. The best News is that it falls back quickly when you stop. On my bike as I get tired the base rate builds up, but that is an encouragement to keep training.
I was talking to á friend about how hills are bit difficult. He, who is 69, replied, “Well you had better perk your muscles up a bit then”

Google tells me that the formula for max pulse is evidently 220 – age (+/- 12) and I seem to be exactly on that limit today at 148 maximum. As a serious CVD victim I though wonder if this is good or bad.

Another thing is how much blood is pumped by each stroke and of course the oxygenation capacity of my “poor” lungs.

Well, well, ones body is a good measuring instrument which tells you a lot about how you feel and where it is located 🙂

Göran
There are other formulas for maximum heart rate which give me a bit more leeway but in general I am over the top. I once spoke to someone whose job it was to test army recruits for maximum heart rate. He told me the formulas are wrong in 50% of the cases.
One last horror story: I was curious to see what my sort of maximum heart rate mine was, so I went on to an athletics track and jogged round a couple of times to warm up. I then ran as fast as I could for 100 metres, and I came up with a maximum rate of 164.
Eugster wrote a book called ” Age is just a number” which is worth reading.
As Dr K kindly wrote ” you are an example of the value of looking after your own health”

Martin, here is a good reason to move:
“The lymphatic system is made up of a network of vessels that carry a clear fluid called lymph throughout the body. Lymph fluid serves the important purpose of carrying nutrients to the cells that bathe in the fluid. The lymph fluid then delivers cellular waste to the bloodstream, which caries it to the kidneys, colon and lungs for elimination. If your lymphatic system is blocked or clogged, you may experience a number of symptoms, including back pain, constipation, fatigue, depression and weight gain. However certain exercises can help release blockages and promote healthy movement of nutrients and waste throughout the body.”

The first one was the first one and whom I met at my very severe MI incident and when I was “totally” ignorant. This first one gratulated me to my “survival”. And he was reasonable all along the five years of our acquaintance and of the checking up and durng my “inauguration” into this science of cardiology after which years he didn’t want to see me any more. He didn’t “argue” when I refused the CABG and not even when refusing all medication. He just told me that everything was OK according to the testing despite my clogged arteries. He even conceded that garlic and omega-3 worked as “anti-cologgants”.

It was the second one I met ten years later that was of another breed and who declared war from the beginning. I think it had all to do with having done my “home work” properly as a researcher and also adhering to the LCHF way of life despite all official “warnings”. Nonsense to his mind.

Ignoring is today a meek word about my feelings towards these “poster-boys” for Big Pharma.

Twenty years ago I belied that what they said was backed up by science so my feelings is today more of having been “fooled”.

Did anyone see the TV programme on ITV yesterday evening (apologies to non UK residents on this board)? It was about health and whether eating fat was bad for you. It was mostly the usual drivel with the “science” presented at the lowest common denominator level with some “experts” and professors seemingly ignorant of their own subject, coming out with dietary advice with no basis in science. I thought I know more than you guys and I’m neither a professor nor a dietician / nutritionist! One scene made me particularly angry. They showed a “fatburg” in a London sewer and described in detail how the fatburg had blocked the sewer. This was done immediately after discussing saturated fat in the diet. After the sewer video clip the presenter said that the body doesn’t quite work like that but… I thought to myself if the body doesn’t “quite work like that”, why show a fatburg blocking a sewer after just having discussed saturated fat in the first place?! The intention was quite clear: it was for the viewer to infer, “artery clogging saturated fat”. It was complete nonsense. Even though they can’t quite bring themselves to actually say, “artery clogging saturated fat” anymore they simply can’t resist almost saying it.

So much opportunity with this type of TV programme to educate the masses yet they repeatedly spout the usual nonsense.

Oh, yes. I sat swearing at the screen in a manner very unbecoming of a 75 year old ‘lady’. I was very disappointed (there’s an understatement if ever there was one) but fully expected the tripe we were fed. It that unfair to tripe?

Mark, It is a real pity when such bad programs are screened. But a few days ago I had the opposite experience with a new science program here in Oz.

I made a comment about it earlier. It is a new Catalyst program about heart surgery hosted by Perth based female heart surgeon Dr Nicki Stamp.

I know that ‘Catalyst’ as a science program may be in bad odour here because of the way that former Catalyst presenter Marianne Delanesi was treated by the ABC management for some of her excellent programs. However the staff at the Science unit of ABC were not responsible for the way she was treated. It was ABC management who did it.

Some interesting points about the program :
1 : The causes of CHD were not discussed at all ..Perhaps this is still too sensitive an issue ?
2 : LDL-C was not mentioned at all; nor was cholesterol or saturated fats. I think that someone was carefully avoiding promoting the idea that they cause heart disease.
3 : There was no attempt to disparage LCHF diets or promote any particular ‘heart healthy diet”.
4 : Exercise was emphasised as necessary to heart health, and was illustrated by 2-3 sequences of Dr. Nicki Stamp jogging as part of her daily personal program to stay healthy.

Oh dear, Mark Johnson – re my reply (below) I watched the wrong programme, though it was very very infuriatingly, banging on about cholesterol and ‘good fats’. They actually classified the picture of an egg as an example of ‘junk food’ – yes really. I tried to find the programme you referred to on catch-up but then decided I didn’t really need to watch another junk programme. So sorry – I must pay better attention and not read these posts while eating my junk food breakfast – scrambled eggs and cheese.

Jan B: I am a junk food breakfaster, too! Three eggs with Grana Padano parmesan grated on top, cooked on top of sauteed onion and garlic, with a bit of smoked salmon and kimchi on the side, and a bit of fruit and chocolate for dessert. It’s a wonder I haven’t keeled over yet!

Oh dear, Gary Ogden, that’s serious. I think you should get medical advice (but only from our very own hero, MK) I need Cheese Eaters Anonymous. My name is Jan and I am a cheese eater.
Excuse me, I must go to the fridge and cut a chunk.

Mark, for some reason we are denied decent and honest scientific documentaries on TV these days. We get odd snippets of info, interspersed with meaningless twaddle. Commentators ‘peddle’ the status quo regarding NHS guidelines, rather than having a serious, in-depth look at current research.
I was annoyed with Channel 4’s ‘Superfoods’ which gave a particularly biased account of consuming raw milk, describing it as a new ‘fad’. This weighted word just trips off the tongue to subliminally indoctrinate the viewer. There is scant evidence that raw milk is unhealthy, yet enough evidence that present day, raw milk is so well monitored as to not cause illness…these facts were brushed aside. The programme did not mention the damage done to the structure of milk resulting from pasteurisation and homogenisation. Let us have more fairness in journalism.
I am fully aware of the controversy surrounding raw milk. But to discredit the good dairymen who provide it for us, by quoting age old statistics about food poisoning, is an insult to the public. It plays into the hands of the producers of processed foods by scaring the s..t out of us. I contend that the de-natured, sanitised, industrial junk they encourage us to consume, is far more dangerous!
Off to enjoy my half pint of raw milk before bed…(had the other sort of tipple an hour ago)

Jennifer: Yes, clean raw milk is a very nutritious food. It has been an epic battle here in the U.S. since Ralph Nader got the ban on interstate shipments of all raw dairy (except cheese aged 60 days). The good news is that in recent years several states have liberalized their raw milk laws in response to actual science and consumer demand. I no longer drink fluid milk, but couldn’t live without raw cream and butter from cows on pasture. Delicious and full of fat-soluble vitamins!

Gary, I am giving you 3 gold stars for your recent postings regarding dairy products and lovely breakfasts. I have completely overhauled my food preparation techniques and eating habits in the last 5 years, with the support of my husband….who spends a lot of time clearing up after me.
Avoiding junk and eating correctly is not a 3 month fad…it is a way of life which takes some determination, but is pays excellent dividends.
By the way, I was critical of the use of research from USA regarding raw milk, but for many years now I have accessed equipment and ideas for food prep from USA, which was not available here in UK. I don’t think the messages get good enough/accurate coverage in our press.

I didn’t see that one but I saw a programm about How To Stay Young. One way apparently, according to the Doctor ( whose name escapes me now, but he’s one of those twin doctors on UK TV a lot) was to make sure you don’t eat the nasty cholesterol which will clog up your arteries and cause you to have a heart attach/stroke. Nice little illustrative film to show how it happens too.

Sue, the problem is that these trashy programmes are, let’s be honest, merely for entertainment…they certainly make me laugh, otherwise I could cry. They are portrayed as factual, which they certainly are not! Dumb-down telly, I call it.
Pleased to see that Dr K partakes of raw milk. As with the word diabetes, ‘raw’ is confusing, but I suspect it is covered under legislation, but I agree, ‘natural’ would sound nicer. I also notice that much of the negativity on the netty, uses stats from USA. It is many years since raw milk caused problems in UK.

Jennifer: In the U.S., too. Very safe if properly produced. Commercial pasteurized milk, on the other hand, can and does sicken and kill. It is all homogenized, too (so the cream doesn’t separate), which oxidizes the cholesterol in the butterfat.

There were a couple of things always in my mind when thinking about atherosclerosis; it seems crucial to incorporate them into an explanation of how atherosclerosis develops . . . So at the initial posting they pushed their way into my mind again.

(A) How pre-atheroma fatty streaks are formed, noting that they can formed in young children.

(B) The vasa vasorum (adventitial capillaries) involvement: Surely this vascular system must come into play, bearing in mind we are dealing with more or less standard capillaries, complete with epithelium (fenestrated to boot) that can provide the artery wall with plenty of things from the blood – good and bad?

On the adventitial capillaries issue . . . I was always been taken with their significance after reading a couple of years ago the work by Ravnskov on “Infections May be Causal in the Pathogenesis of Atherosclerosis”. He described the adventitial capillaries as the route of infection into the artery wall, and that infection was the initiating event for the subsequent plaque development.

The Subbotin paper was a revelation, a revelation grounded in many anatomical studies of cardiac arteries.
He agrees with the majority of researchers that a cardiac artery has 3 significant cellular layers, (ignoring separating elastic membranes) . . .
The intima layer (often described as single cell deep endothelium layer plus underlying proteoglycan matrix),
The media layer (smooth muscle cells and elastic fibres)
The adventitia layer (connective tissue)
Coming through the adventitia and into the media layer you have the adventitial capillaries – providing for the nutritional demands of the smooth muscle cells in the media layer.

But Subbotin and others differ with parts of the above . . .

They say that the intima layer might start off a single layer of tightly bound epithelial cells . . . but as a person ages the intima thickens, by intimal cells dividing. Typically the coronary tunica intima of young children (8.5 months) consists of only 1-2 layers of cells lying on a thin amount of matrix and internal elastic lamina, reaching 10-15 layers at age 15. Leading to approximately 25-30 cell layers at age 25-30 years.

The intimal cells are supplied nutrients/oxygen by diffusion from the artery lumen. (issue here)
This becomes more difficult for the intimal cells farthest from the lumen as the intimal layer gets thicker.
They suggest that the intimal cell are fully able to proliferate when required.
If proliferation occurs the intimal layer gets thicker and the outer intimal cells begin to lack oxygen.
Distress signals are sent out to which to the adventitial capillaries respond and start developing into the intimal layer.
Only to be found in the outer intima, parts farthest from the lumen, are biglycans (part of the proteoglycan matrix that bind particularly strongly with LDL particles) . . . thus LDL can concentrate in this deep region.
You now have a fatty streak . .. and the potential site of a future plaque.
He sees the future plaque growing from the outside to in, towards the lumen, in a sense fed by its blood supply.

He sees that up to the fatty streak lesion stage the situation is reversible . . . presumably macrophages easily infiltrate can do some tidying and removing bound LDL – via adventitial capillaries.

The central point is that something causes proliferation of the intimal cells, and this intimal thickening leads to invasion of adventitial capillaries into the intima – Initially > fatty streaks, later possibly > atheroma.

They would suggest that biomechanical/hydraulic effects in the moving heart produce areas of low shear stress, low NO concentration and these can stimulate intimal proliferation. These areas coincide with plaque formation.

One observation that fits the model: The development of the fibrous cap of a plaque described as involving the migration of smooth muscle cells from the disrupted media to above the lipid mass seemed a bit far fetched. In the above model the elements of the elements of the fibrous cap are already there.
There are other supporting observations described in the paper.

Does this explain how guinea pigs depleted of vitamin C can develop atherosclerotic plaques within days? Also, if endothelial cells can proliferate, why does the bone marrow produce Endothelial Progenitor Cells. To me, he is using circular logic. ‘We find that there can be several layers of endothelial cells, which means that they must be able to proliferate.’ ‘How do you know they can proliferate?’ Well, look, there are several layers, so they must have proliferated.’

Maybe some of the endothelial cells are dead cells which have reached the end of their useful life, but the clean-up process isn’t functioning efficiently and they remain in place instead of being removed.

In the few papers I have read, Subbotin does not talk about where the extra intimal cells below the epithelial cell layer come from. I must say it did seem odd and screamed out for an explanation; however, without one, I assumed (ouch) that the epithelial cells must have a different phenotype to the putative cells of the intimal body. It is the intimal body cells that must be doing the proliferating, presuming that the epithelial cells have enough of a demanding job already. (The endothelium proper will still need the endothelial progenitor cells for essential repair)

The Figure 7 of the paper I mentioned shows a schematic of his idea of the artery composition, which has the intimal body cells embedded in a proteoglycan matrix, spaced apart, not in clear layers, quite separate from the epithelial cells.

Where the initial intimal body cells originated is unstated . . . but it does seem that the number, according to some, does appear to increase with age, and particular areas of low shear stress, and they put this down to activated cell proliferation of the intimal body cells.

The lack of vitamin C, as I understand it, will compromise the functioning of epithelia and damage their integrity. But, ever since coming across Ravnskov’s work, whenever some damaging agent to the artery lumen endothelium was proposed . . . I could just as easily see it damaging to the epithelia in adventitial capillaries.

I could conceive of two situations . . . epithelial damage of the artery lumen by Vit C lack . . causing an occlusive blood clot in lumen resulting in a heart attack. At the other end, the damage to the adventitial capillary epithelium will cause leaking into the media and/or intimal layers, setting up a significant inflammatory reaction. Proteoglycans hanging on to LDL would not help. You end up with a lipid core atheroma . . . which can grow, being ‘fed’ by the adventitial capillaries. . . leads to lumen occlusion . . . as the atheroma grows it pushes into the luminal epithelium . . . now luminal epithelial integrity is important . . . If it is compromised . . .> thrombus . . . > heart attack.

I do realise that what have written is a bit of a house of cards built on scattered, very incomplete knowledge. I greatly appreciate your indulgence of these musings.

I aways thought of an artery like a plastic hose pipe, with a smooth black inner lining, an outer green casing, and fibre reinforcing. If you look at diagrams, the inner lining (intima) is always a smooth, thin layer.

But if you look at actual cross-sections of an artery photographed under a microscope, the intima has a very wrinkled appearance. It resembles the surface of the brain more than a smooth layer. I’m getting confused.http://www.anatomybox.com/muscular-artery/

I sort of agree if by “balance” you mean comments by the presenter such as, “we shouldn’t be getting rid of entire food groups [carbohydrates] because of the danger of nutrient deficiency when she should have at least qualified that by saying that our actual need for carbohydrate is zero, unlike fat and protein. And whenever saturated fat is mentioned they always show a picture of a doughnut, biscuits or a piece of cake. So it isn’t the denatured flour or sugar or fake fat (margarine made from who knows what) in the doughnut which is then fried in the crappiest, cheapest vegetable oil available that’s the problem, but “saturated fat”. It’s this sort of “balance” that I have a problem with. Or the dieticians harping on about calories and how we should go easy on the fat because it has 9 calories / g as opposed to carbs which have 4. In the end the average viewer just thinks it’s all about the calories and a “balanced diet” while in the meantime putting on the pounds year by year.

I was referring more to the comments by Zoe Harcombe, and some others. If you pick only the news you mentioned then the program will appear biased. I accept there are a lot of crap statements, and some of which you mention, which makes the program look like a load of rubbish.

As soon as I dig into “anything” in our physiology I am as you getting confused due to the complexity which is revealed the deeper you dig. The good thing about doing this is though that you don’t believe in “one-liners” like “take your statins” anymore 🙂

Your apt input here also reminds me of what I read in the classic Joslin’s “Diabetes Mellitus”, though in an old edition (1970), and where, with the use of an electron microscope, capillaries were studied and it was stated that the “surest” early sign of diabetes was that the lamina surrounding these capillaries had been narrowed. My guess reading this was that this narrowing is due to an inflammatory process related to high glucose levels.

Martin, my understanding is that the relative thickness of various layers depends on where the artery is located: coronary artery different to say a brachial artery. The diagram you show may work well as a generic example of an artery, but I am not sure it represents say the Left Main Coronary artery?

I think the micrographs shown in figure 3 in “Early Human Atherosclerosis Accumulation of Lipid and Proteoglycans in Intimal Thickenings Followed by Macrophage Infiltration”http://atvb.ahajournals.org/content/27/5/1159.long 2007
. . . present a different story.

They are reproduced in the Subbotin paper. The paper gives many more references over the past 80+ years of histological studies on coronary arteries that show an intimal layer more than 1 cell layer thick . . . naturally thickening with the demands on the heart inside a growing body.
It is worth having a look at the paper.

Dr Kendrick cannot provide individual patient advice over the Internet. UK General Medical Council regulations are clear that to do so would be a breach of medical standards that could result in disciplinary proceedings.

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